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This post is a guide only and should not be taken as medical advice. It does not replace assessment and recommendations from a registered and regulated healthcare professional.

So, a child’s scan has come back with something called a Schmorl’s node.

First thought: “What on earth is that?”
Second thought: “Is this bad?”
Third thought: “Why does it sound like the name of a minor Harry Potter villain?”

Fair enough.

Schmorl’s nodes are real. They can matter. But most of the time they are more interesting than ominous.

Before we get to them properly though, we need to talk about the structure they come from.

Meet the Disc

Ah yes — the disc.

Its reputation precedes it. It’s a party animal apparently, it allegedly “goes out” a lot.

Unfortunately, it has spent decades being cast as the main villain in every back pain story. Radiology reports have helped a bit, but they’ve also helped create generations of people walking around saying things like, “My GP told me I’ve got three slipped discs” while holding an MRI that mostly shows very normal age-related changes that many painless humans also have.

So before the disc gets blamed for yet another crime it may or may not have committed, it helps to introduce it properly.

Between each spinal bone sits an intervertebral disc. Think of it as a pressurised gel cushion sitting between two vertebrae.

It has three main parts:

• a softer, hydrated centre called the nucleus pulposus

• a tough outer rim made of layered rings called the annulus fibrosus

• and the endplates on the top and bottom, which form the interface between the disc and the vertebral bone (1)

  

Tom Jesson describes the disc beautifully as a force distributor, not just a “shock absorber.” The nucleus helps spread load outward into the annulus. The annulus is built to handle that outward spread of pressure. The endplates, however, are less well suited to dealing with vertical intrusion from above or below (1).

That’s the key concept for this whole article:

For Gen Z and younger, here’s another way of explaining it:

For those who are Umbilicus fans, it’s the opposite of belly buttons, in this instance: Outie’s are cool, Innie’s are not.

So when we’re talking about Schmorl’s nodes, we are not talking about the usual “disc pushes backwards and annoys a nerve” storyline.

We are talking about something else entirely.

So What Is a Schmorl’s Node?

A Schmorl’s node is a type of vertical disc herniation.

Instead of disc material pushing backwards or sideways, some of the disc material pushes upward or downward through the endplate into the bone of the vertebra above or below (3, 4)

So if the more familiar disc herniation story is:
“disc material went out the side door”

then the Schmorl’s node version is:
“disc material went upstairs or downstairs.”

It can leave a crater-like or dimple-like defect in the vertebral endplate. On imaging, it can look dramatic. Clinically, it is often much less dramatic than the scan suggests.

Are They Always Painful?

No.

And this is where it gets important, because this is also where scans can spook families and junior clinicians alike.

Schmorl’s nodes are found in people with pain and in people without pain (4). So like plenty of imaging findings, they can be:

• the cause

• part of the story

• or just a witness standing awkwardly at the scene

That said, in children and adolescents they can absolutely be symptomatic, particularly when they form more acutely or when there is active inflammatory change in the surrounding bone (4, 6).

That is where MRI becomes more useful than just saying, “Yep, there’s a Schmorl’s node.”

If the bone around the node is oedematous and lit up, it is much more likely to be new and grumpy rather than an old silent footprint.

At this point, the question isn’t ‘is there a Schmorl’s node?’
It’s whether it actually matters.

This is where the real clinical thinking starts.
The difference between “tight and weak” and “something actually going on” is what separates a plan from a guess.

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This post is a guide only and should not be taken as medical advice. It does not replace assessment and recommendations from a registered and regulated healthcare professional.

There is a certain type of musculoskeletal consult that should make you sit up a bit straighter.

The patient has calf pain, thigh aching, buttock heaviness, or a vague “my legs just feel rubbish” complaint - on both sides.

The loading story is underwhelming - there wasn’t a ‘too much, too soon’ moment. The objective findings are not useless, but they are not exactly pointing neatly to one clean diagnosis either.

The pattern is a bit too bilateral, a bit too diffuse, or a bit too grumbly to sit nicely in the usual tendon-joint-spine buckets.

They’ve already had a bucket-load of previous “physio” on them (the needling, the massage, the cupping, the zapping, the scraping), unsurprisingly with the same short term results: “Feels good but it comes back… oh and it’s expensive going back all the time”.

So you start thinking:

“Is this lumbar canal stenosis? Deconditioning? Something systemic maybe? Peripheral arterial disease?”

But sometimes the answer is sitting there quietly in the subjective, hiding in plain sight between the antihypertensives and the vitamin D.

Statins.

Not because statins are evil. Not because every sore calf in a 62-year-old is suddenly pharmacological. But because if you do not ask about medications and timing of new prescriptions, you can miss a perfectly reasonable differential and spend weeks trying to rehab a problem that is not behaving like a normal musculoskeletal one for a very good reason.

Differential Diagnosis tip: “If it’s both sides - look in.”

If there’s peripheral (arms and legs) symptoms on BOTH limbs, clear systemic or spinal causes.

Example: If it seems like bilateral golfers elbow - it’s highly unlikely - think Cervical Radicular Pain. If it seems like it’s bilateral insertional Achilles tendinopathy - clear the system (and also consider auto-immune inflammatory conditions).

This Is Not an Anti-Statin Blog

Statins are important drugs.

They reduce LDL cholesterol, lower cardiovascular morbidity and mortality, and remain a major part of vascular risk reduction (1). They also appear to do more than just nudge lipid numbers around, they can have positive effects on plaque stability, endothelial function, inflammation, and oxidative stress (2).

So this is not a “statins are bad” blog.

This is a “physios should be better at spotting when the story doesn’t quite add up” blog.

Why Physios Should Care

Musculoskeletal pain is common. Statin use is common. Low back pain and lower-limb pain are our bread and butter. Which means statin-related muscle symptoms can hide beautifully in MSK practice if we are not awake to it.

Studies have found that statin users aged 40+ without arthritis were more likely to report musculoskeletal pain, particularly in the lower back and lower limbs, than non-users (1, 3).

That matters, because lower-limb pain and back pain are exactly where ‘business-as-usual assumptions’ breed. Tight calves. Weak glutes. Just ageing. A bit of back referral. Probably the hammy.

Business as usual? Sometimes yes.

But sometimes the clue is that the patient started or changed a statin a few weeks ago and nobody asked.

What Are Statins Used For? And Why They Still Matter

Statins are primarily used to reduce LDL cholesterol and lower cardiovascular risk, particularly in primary and secondary prevention of atherosclerotic disease (1, 2).

That matters when talking about side effects. If a patient may be experiencing statin-related pain, the correct response is not to become a backyard cardiologist and tell them to bin the script.

The correct response is to recognise the possibility, understand the pattern, and direct them back to the prescribing doctor for review.

Because these drugs often do important work.

What About Peripheral Arterial Disease?

This is where the conversation gets more interesting.

Statins are not just beneficial for coronary disease on paper. In people with peripheral arterial disease, statin use has been associated with better lower-limb function, including improved 6-minute walk performance, faster walking speed, and better overall performance scores. There is also evidence of a 38% reduction in new or worsening intermittent claudication over a median 5.4 years (4).

That is a useful reminder that statins may be part of the solution in one lower-limb presentation while also being part of the differential in another.

Both can be true.

When Does Statin-Related Muscle Pain Usually Show Up?

This is the practical question most relevant to physios.

Does statin-related muscle pain tend to start quickly after starting the medication, or can it just appear years later out of nowhere?

Statin-related muscle pain has most commonly been reported to show up within about four weeks of starting the medication.

Symptoms that begin within that window, then settle within two to four weeks of coming off it, fit the more classic pattern. Symptoms that appear much later, or just linger on and on, are less typical (2).

That is clinically useful.

If someone says, “I started this statin four years ago and this pain began last Tuesday,” that is not the neat, textbook pattern for typical statin-related sore muscles. It does not rule it out, but it should make you ask what changed recently. Dose increase? New medication mix? Illness? Thyroid issue? Kidney issue? Sudden jump in training load?

So the fair summary is this: classic statin-related muscle symptoms usually show up within weeks of starting the medication or increasing the dose. Pain first appearing years later is less typical, and should push you to look for another trigger or another diagnosis (2).

What Does It Tend to Look Like?

One reason this gets missed is that statin-related pain does not always behave like tidy local tissue pain.

Typical statin-associated symptoms are usually bilateral and involve larger muscle groups such as the thighs, buttocks, back, and shoulders.

Cramping may affect smaller muscles and can be unilateral, but the more classic pattern is broad, proximal, and non-specific (2).

The patient may describe heaviness, aching, cramping, weakness, fatigue, or a general sense that their legs are “just not right.” The history may not be strongly load-dependent. The exam may find something, but not enough to fully explain the story.

It may even be a not-so-spontaneous joint effusion, some case studies exist reporting knee effusions linked with patients starting on statins (5).

That is when the medication history stops being background admin and starts being part of the assessment.

Who Is More At Risk?

Risk factors for statin-associated muscle pain include:

• Having them before (duh!)

• Unexplained cramps

• Elevated CK

• Family history

• Untreated hypothyroidism

• Older age

• Frailty/small body frame

• Multisystem disease

• Alcoholism

• Major surgery

• Excessive physical activity, and

• Drug interactions (2).

So your higher-risk patient might be older, frailer, more medically complex, hypothyroid, recently put on a higher dose, or taking another medication that makes the statin harder to tolerate.

In other words, not every sore leg is just a sore leg.

Sometimes it is a sore leg with a medication subplot.

The Subjective Question That Matters

This is the useful bit.

Do not just ask, “What medications are you on?”

Ask, “Have there been any recent changes to your medications around the time this started?”

That is a far better question.

Because patients often do not volunteer dose changes, medication swaps, recent antibiotics, antifungals, thyroid issues, or other relevant changes unless you drag the timeline into the room.

A useful version might sound like this:

“Any new meds, dose increases, or medication changes in the few weeks before this started? Especially cholesterol tablets, antibiotics, antifungals, or anything else your GP changed?”

That one question may save you from spending four sessions solemnly rehabbing ‘tight calves’ that just so happened to appear the same month the statin dose doubled.

What Physios Should Watch For

Your suspicion should rise when the pain is bilateral, diffuse, heavy, crampy, weak, or oddly out of proportion to the loading story.

Your suspicion should rise when the patient cannot give you a convincing mechanical trigger.

Your suspicion should rise when symptoms started within weeks of the patient starting a statin or having the dose increased, especially when the patient is older, frailer, hypothyroid, medically more complex, or taking other interacting medications.

The pattern most suggestive is symptoms coming on while they’re on the statin, settling after stopping it, then returning if the medication is tried again (2).

That does not mean physios should be telling patients to stop their meds and see what happens. But it does mean we should recognise the pattern, document it properly, and send the patient back to the prescriber with a sensible note rather than blindly doubling down on a local tissue explanation that is not behaving.

The Practical Take-Home

Statins are useful medications. Often very useful.

They can reduce cardiovascular events, may improve lower-limb function in PAD, and should not be casually villainised (2-4).

But they can also complicate the musculoskeletal picture.

Symptoms usually appear early, often within weeks of starting therapy or increasing the dose, rather than popping up years later for no reason.

When pain shows up much later, it is less typical and should make you think about new triggers, interactions, or alternative diagnoses rather than reaching for a lazy conclusion.

So if the story feels vague, bilateral, heavy, crampy, or just a bit off, ask about recent medication changes.

Because sometimes the most important differential diagnosis in an MSK consult is not exotic.

Sometimes it is just sitting there quietly between “rosuvastatin 20 mg” and “take one at night.”

References

1. Buettner C, Rippberger MJ, Smith JK, Leveille SG, Davis RB, Mittleman MA. Statin use and musculoskeletal pain among adults with and without artitis. The American journal of medicine. 2012;125(2):176-82.

2. Pergolizzi Jr JV, Coluzzi F, Colucci RD, Olsson H, LeQuang JA, Al-Saadi J, et al. Statins and muscle pain. Expert Review of Clinical Pharmacology. 2020;13(3):299-310.

3. Buettner C, Davis RB, Leveille SG, Mittleman MA, Mukamal KJ. Prevalence of musculoskeletal pain and statin use. Journal of general internal medicine. 2008;23(8):1182-6.

4. McDermott MM, Guralnik JM, Greenland P, Pearce WH, Criqui MH, Liu K, et al. Statin use and leg functioning in patients with and without lower-extremity peripheral arterial disease. Circulation. 2003;107(5):757-61.

5. Campion J, Western A. Statins and joint pain. British journal of clinical pharmacology. 2008;66(4):570.

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After publishing “What Is All This ‘Tightness’ and ‘Stiffness’… and Does It Actually Matter?”, I had a subscriber reach out with a very fair follow-up question:

“Okay — I agree with the concepts. But how do you actually apply this in the clinic?”

It’s a good question.
And an important one.

Understanding that tightness and stiffness are sensations, not tissue read-outs, is one thing. Translating that knowledge into real conversations, real assessments, and real treatment plans — without turning every appointment into a belief-correction exercise — is something else entirely.

This post is the practical companion to that earlier piece.
Not more theory. Not more debate.

Just how I actually handle this — what I say, what I don’t say, and why — in real clinics, with real patients who have often spent years being told they’re “tight” and need fixing.

If you haven’t read the original post, start there:

First principle: don’t mention the Kool-Aid

(and resist the urge to prove how much you know)

Early in your career — or any time you meet a new patient — it’s easy to feel like you need to gain credibility.

That often shows up as:

• over-explaining

• correcting language too quickly

• subtly (or not so subtly) telling people they’re wrong

Even when well-intentioned, this can backfire.

You are not going to change deeply held beliefs in the first appointment.
Don’t try.

If it happens organically — great.
But chasing it is usually counterproductive.

The first session isn’t about winning an argument.
It’s about safety, trust, and a plan that works.

Often the most effective strategy is simply to not reinforce the belief, and to let experience quietly do the work.

🔒 Paid subscribers section begins here
The rest of this post goes into the practical side — the language I use, the metaphors that work, and how I apply this thinking in real clinics with real patients.

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The Claims That Started It All

There are two phrases that have probably done more cultural damage in musculoskeletal care than any others:

“You’re really tight.”
“Wow — you’re very stiff through here.”

They sound scientific.
They feel explanatory.
They definitely justify ongoing treatment.

But here’s the uncomfortable truth:

Tightness and stiffness are sensations — not diagnoses.
And they are poorly correlated with tissue status.

That statement isn’t ideological.
It’s empirical.

Tightness Is a Sensation, Not a Tissue Indicator

“Tightness” and “stiffness” are subjective perceptual experiences, generated by the nervous system.

They behave like:

• pain

• fatigue

• effort

• breathlessness

They fluctuate with:

• context

• expectation

• attention

• threat

• prior experience

• what a clinician has just told you about your body

A sensation is real — but it is not a mechanical measurement.

This distinction matters, because once a sensation is mistaken for a tissue fault, the entire narrative of care shifts toward “fixing” something that may not be broken.

Research Review | Do “Tightness” and “Stiffness” Reflect Tissue Status?

When “tightness” and “stiffness” are treated as mechanical findings, the implicit assumption is that they reflect measurable properties of muscle or joint tissue.

When those properties are actually measured, that assumption doesn’t hold up well.

1. Muscle hardness is poorly related to pain or stiffness

Objective measures of muscle hardness do not reliably correspond with pain sensitivity or perceived stiffness.

Painful regions are often not the hardest, and increases in tenderness do not imply increased tissue hardness. This challenges the idea that “tight” tissue is mechanically abnormal or pathological.

(Andersen et al., 2010, Andersen et al., 2006)

2. Changes in tissue properties do not track with symptom change

Even when interventions produce measurable reductions in muscle hardness, those changes show weak or no correlation with improvements in pain, disability, pressure pain thresholds, or perceived recovery.

Symptoms may improve, but not in proportion to — or because of — measurable tissue changes.

(Somphithak et al., 2025)

3. Feeling stiff is not the same as being mechanically stiff

Perceived stiffness frequently fails to align with objective measures of mechanical stiffness or range of motion.

Individuals may report high stiffness despite normal movement and mechanical properties, while others demonstrate movement restriction without feeling stiff.

(May et al., 2017, Stanton et al., 2017)

4. Body perception plays a major role in symptom experience

People with similar physical findings can report very different levels of stiffness and pain.

This variability is better explained by differences in sensory processing, central sensitivity, and body perception than by structural tissue differences alone.
(Viceconti et al., 2020, Funabashi et al., 2022, Arendt-Nielsen and Graven-Nielsen, 2008)

Summary of the Evidence

Across multiple research domains:

• Tightness and stiffness are subjective sensations

• Objective tissue measures show weak and inconsistent correlation

• Changes in tissue properties do not reliably predict symptom change

• Perception, context, and nervous system processing play a substantial role

This is what is meant — precisely — by “poorly correlated with tissue status.”

So How Did This Get So Out of Hand?

Here’s where things stop being accidental.

Somewhere along the way, the musculoskeletal industry stopped treating “tightness” as a symptom….
and started selling it as a problem.

Not because the evidence demanded it, but because the reimbursement model rewarded it — and in some healthcare systems, such as the itemised U.S. insurance model, it is explicitly billable.

As an Australian I should probably be VERY careful criticising the U.S. reimbursement model — apparently “national security” has a very flexible definition these days, and Tasmania is looking awfully strategic, especially with that oil sitting just north of it in Bass Strait.

“But I Can Feel It” — The Trigger Point Industrial Complex

As outlined in Attack of the Trigger Points: When Poking Becomes a Profession, a very obvious pattern emerges:

👉 Those who believe tightness and stiffness matter most
👉 are often those who make their living from ‘untightening’ and ‘unstiffening’ people

This isn’t malice.

It’s the Law of the Instrument:

If all you have is a hammer, everything looks like a tight muscle.

Needles see trigger points.
Thumbs see knots.
Alignment specialists see crookedness.

And “tightness” becomes the universal justification.

The Metaphorical Monorail Problem 🚝

Here’s the truly awkward part:

Most of these approaches work — temporarily.

Not because tissue was structurally “released”, but because of contextual effects.

• confident explanations

• plausible stories

• therapeutic ritual

• expectation of benefit

This is the Monorail Model of Care:

• compelling narrative

• short-term relief

• no exit strategy

Patients feel better — until they don’t.
Then they return for more “maintenance”, not because their body is failing, but because the story told them it would.

The Real Damage: Public Literacy

This is where it genuinely matters.

When the public is taught that:

• tightness equals damage

• stiffness equals dysfunction

• relief requires ongoing “release”

we don’t create informed patients — we create dependent ones.

People stop trusting movement. They outsource confidence. They become hyper-vigilant to normal sensations.

All because a sensation was sold as a structural defect.

This Is Not Anti–Manual Therapy (Read This Slowly)

Let’s be clear:

❌ This is not “manual therapy does nothing”
❌ This is not “stretching is useless”
❌ This is not profession-bashing

I’m not looking for a Straw-Man War.

Manual therapy can:

• reduce pain

• calm symptoms

• restore confidence to move

But when it’s framed as structural correction instead of sensory modulation, it becomes misleading.

Feel-good care is fine.
Just don’t dress it up as tissue repair.

Why This Is So Frustrating (and Why It Matters)

What frustrates many of us who work in this space — and who are familiar with this evidence — is not that patients develop these beliefs in the first place.

That part is easy to understand.

When:

• authority figures speak confidently

• explanations sound anatomical and scientific

• short-term relief follows

• and the narrative is repeated often enough

people do exactly what humans are wired to do: they form beliefs that make sense of their experience.

The problem is what happens next.

Once someone adopts the belief that their body is structurally tight, stiff, out of alignment, or in need of ongoing “release”, it becomes extremely hard to undo. Not because patients are foolish — but because belief revision is neurologically, emotionally, and socially costly.

Exiting that belief system — “leaving the cult,” for want of a better phrase — takes:

• time

• careful explanation

• repeated exposure to contradictory experiences

• and, often, unlearning fear before learning anything new

That work is far harder than planting the belief in the first place.

And it’s work that usually falls to clinicians who are trying to rebuild confidence, restore autonomy, and reduce dependency — often while simultaneously addressing pain, disability, and frustration that have accumulated along the way.

That extra work has real costs:

• more appointments

• longer treatment timelines

• higher out-of-pocket expenses for patients

• greater costs to insurers

• and, ultimately, higher expenditure for taxpayers

All because a sensation was framed as a structural defect.

This is why public literacy matters.
Not because we want to “win an argument”, but because beliefs shape suffering — and poorly grounded beliefs are expensive for everyone involved.

The Actual Takeaway

• Tightness is a sensation, not a tissue diagnosis

• Stiffness is a perceptual experience, not a mechanical read-out

• Their link to tissue status is weak and inconsistent

• Overselling them distorts public understanding and fuels dependency

So what now….?

Part two is practical guide to applying the evidence without burning yourself out.

References

• Andersen, H., Arendt-Nielsen, L., Danneskiold-SamsØe, B., & Graven-Nielsen, T. (2006). Pressure pain sensitivity and hardness along human normal and sensitized muscle. Somatosensory & motor research, 23(3-4), 97-109.

• Andersen, H., Ge, H.-Y., Arendt-Nielsen, L., Danneskiold-Samsøe, B., & Graven-Nielsen, T. (2010). Increased trapezius pain sensitivity is not associated with increased tissue hardness. The journal of Pain, 11(5), 491-499.

• Arendt-Nielsen, L., & Graven-Nielsen, T. (2008). Muscle pain: sensory implications and interaction with motor control. The Clinical journal of pain, 24(4), 291-298.

• Funabashi, M., Wang, S., Lee, A. D., CK Duarte, F., Budgell, B., Stilwell, P., & Hogg-Johnson, S. (2022). Discomfort, pain and stiffness: what do these terms mean to patients? A cross-sectional survey with lexical and qualitative analyses. BMC musculoskeletal disorders, 23(1), 283.

• May, E. S., Tiemann, L., Schmidt, P., Nickel, M. M., Wiedemann, N., Dresel, C., . . . Ploner, M. (2017). Behavioral responses to noxious stimuli shape the perception of pain. Scientific reports, 7(1), 44083.

• Somphithak, S., Chatchawan, U., Pimdee, A., & Sucharit, W. (2025). Reliability and responsiveness of a tissue hardness meter and algometer for measuring tissue hardness and pressure pain threshold in upper trapezius myofascial trigger points. PeerJ, 13, e19580.

• Stanton, T. R., Moseley, G. L., Wong, A. Y., & Kawchuk, G. N. (2017). Feeling stiffness in the back: a protective perceptual inference in chronic back pain. Scientific reports, 7(1), 9681.

• Viceconti, A., Camerone, E. M., Luzzi, D., Pentassuglia, D., Pardini, M., Ristori, D., . . . Testa, M. (2020). Explicit and implicit own’s body and space perception in painful musculoskeletal disorders and rheumatic diseases: a systematic scoping review. Frontiers in Human Neuroscience, 14, 83.

Related Reads

PainScience.com - Paul Ingraham

• You’re Really Tight Doesn’t Mean Much — Explores how feelings of tightness are poorly linked to tissue mechanics and why the common interpretation of “tight” lacks evidence.
  https://www.painscience.com/articles/youre-really-tight.php

• Stiffness and Range of Motion — Discusses the relationship (or lack thereof) between subjective stiffness and objective range of motion, and clarifies common misconceptions.
  https://www.painscience.com/articles/stiffness-and-rom.php

My Ramblings

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Why I’m Writing This

There’s a pattern I see repeatedly in second-opinion consultations for ulnar-sided wrist pain.

If a patient has been told they have a “TFCC tear”:

• without imaging

• without a clear traumatic mechanism

• and without convincing signs of instability

I usually don’t learn much about the wrist —
but I do learn something about the context the diagnosis was made in.

Not malice. Not laziness.
Just a very common situation where wrist pathology is unfamiliar, complex, and uncomfortable to reason through.

TFCC is quietly becoming what piriformis syndrome was 10–15 years ago:
a placeholder diagnosis — a confident-sounding label used when certainty outpaces evidence.

A Common Clinical Conversation

A common request I get from clinicians — particularly those who haven’t spent time in hand therapy — goes something like…:

“How do you manage TFCC injuries?”

My response is usually:

“How do you know it’s TFCC in the first place?”

There’s often a short pause — the kind of thousand-yard stare every clinician recognises — before the realisation lands and they say, sometimes out loud:

“Actually… I don’t.”

That moment matters.

Not because anyone has done anything wrong, but because it exposes how easily TFCC becomes a diagnostic crutch when the ulnar wrist feels complex and unfamiliar. Very often, the better question isn’t how do I manage a TFCC injury? — it’s am I justified in calling this TFCC at all?

Once that’s acknowledged, management usually becomes simpler, more honest, and far more effective.

Experience Doesn’t Add Diagnoses — It Takes Them Away

Much like deeper study and experience in lumbosacral and hip pathology eventually weans clinicians off reflexively using piriformis syndrome for anything that can’t explain, the same thing happens with the wrist.

The ulnar side of the wrist is anatomically complex — layered structures, overlapping pain patterns, shared loading mechanisms — yet the early management is often quite simple.

The catch is this:

It takes a complex understanding to earn simple management.

After thousands of wrist and hand presentations, time working in hand therapy, and regular collaboration with hand and wrist orthopaedic specialists, I gradually stopped telling patients:

“You’ve torn your TFCC.”

Not because TFCC injuries don’t exist —
but because I finally understood how rarely that statement is defensible.

Despite working across rugby, tennis, track & field, and general sport, the total number of confirmed, symptomatic TFCC tears I’ve personally managed in over a decade of practice is:

Zero.

That’s not a flex.
It’s a clue.

Why Most of Us Rarely See True TFCC Tears

True TFCC injuries are usually:

• traumatic

• high-force

• often associated with distal radius fractures

  

These patients don’t drift into routine MSK clinics.

They go:
ED → imaging → orthopaedics → surgery → hand therapy

Which means most general MSK clinicians simply don’t see them often.

And even when TFCC injury exists alongside a distal radius fracture, immobilisation alone is frequently enough to restore function and reduce symptoms to clinical irrelevance.

Diagnostic Reality Check

Even MRI can get it wrong. I didn’t know this until my local Hands Specialist/Surgeon told me:

“Nick…. they look like a TFCC on the scan, but then we get in there (surgery) and it’s the LT ligament (lunotriquetral ligament)” - and vice versa.

It can look like a TFCC but be a LT lig, it can be an LT lig but be a TFCC - or neither at all.

So diagnosing a symptomatic TFCC tear:

• clinically

• without trauma

• without imaging….. and perhaps without surgery

isn’t diagnostic confidence — it’s false certainty.

Why the Label Matters

Using TFCC as an umbrella term for ulnar wrist pain:

• anchors patients toward surgical narratives, or to wearing wrist supports long-term (“or else”)

• increases threat perception -

• narrows rehab tolerance

• and doesn’t change early management anyway

  

If the diagnosis can’t be confirmed — and wouldn’t alter management —
why name it at all?

This is why I default to terms like:

• ulnar-sided wrist pain

• ulnar compartment irritation

• ulnar compartment effusion / overload

The same way we talk about:

• posterolateral corner irritation of the knee

• lateral elbow pain rather than “tennis elbow”

So What Does the Research Say?

Short answer: it strongly supports this position.

Across imaging, surgical, and review literature:

• TFCC tears are uncommon and usually traumatic

• MRI has meaningful limitations, even at 3T

• arthroscopy is invasive and reserved for select cases

• many TFCC tears do not require treatment

• ECU tendon pathology is more common in athletes

• conservative management is first-line in most cases

Across work by Deniz (2013), Pang (2017), Jawed (2020), and Zhan (2020), the same message appears repeatedly:

TFCC is real — but it is rare, difficult to confirm, and frequently overdiagnosed.

Assessment: Keep It Honest

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Persistent elbow pain in your child is not “tennis elbow.”
Kids don’t wear out tendons — they stress their growth plates, cartilage, and bone anchors.

• Red flags: catching, locking, swelling, loss of extension.

• Good news: Most of these conditions improve with rest and careful load management.

• Next step: Seek a provider with specific training in paediatric and adolescent sports injuries. This isn’t guaranteed in every clinic.

No — that child isn’t balding.
No — that child isn’t going grey.

And just as we don’t expect children to show adult patterns of ageing, we shouldn’t expect them to present with adult tendon disorders.

Kids don’t get plantar fasciitis.
They don’t get degenerative rotator cuff tears.
And they don’t get “tennis elbow.”

Because kids don’t get rope problems.
They get anchor problems (apophysis).
They get foundation problems (bone).
And growing kids (unsurprisingly) get growth plate problems.

This is especially true in the athletic child. Repetitive loading from throwing, tumbling, serving, or impact doesn’t fray tendons the way it does in adults. Instead, it stresses the growth centres, the anchors, and the foundations of the developing skeleton. That’s where overuse injuries live.

In this blog, I’m not going to cover Medial Elbow Pain in active kids, such as Little Leaguers Elbow (https://kidsback2sport.com/educate/little-leaguers-elbow-what-parents-need-to-know/). This condition is the most common cause of elbow pain and is less commonly missed. It’s also technically it’s on the complete OTHER side of the elbow to “Tennis Elbow” – and is usually pretty clearly presenting as ‘medial elbow pain’.

Why Correct Diagnosis Matters

Getting the diagnosis right in young athletes is important because it directly guides safe, effective exercise selection and helps kids return to sport confidently and without unnecessary setbacks.

For example, if a child has a traction apophysitis, stretching is not just unhelpful — it can add more traction to an already irritated growth plate. Similarly, if a young athlete has olecranon apophysitis, exercises that load the triceps (like pushdowns or dips) won’t support healing because the triceps pull on the very area that needs time to settle.

A correct diagnosis also lets us set the right expectations around rest. When children develop growth plate or bone-stress injuries, they usually need complete rest from the aggravating activity — not just “dialing back a bit.” Complete rest allows the bone, cartilage, and growth centres to recover fully, so they can return to sport stronger and safer.

This is why understanding paediatric elbow conditions matters so much. Young athletes aren’t smaller adults, and adult protocols don’t always fit their biology. With the right diagnosis, we can choose the right exercises, avoid the wrong ones, and give kids a clear, confident pathway back to the activities they love.

If we get this right, kids heal well, stay active, and continue enjoying their sport — which is exactly what we want.

Imaging Principles

• MRI → investigation of choice for paediatric overuse injuries. It avoids ionising radiation and best visualises marrow, cartilage, and growth plates (1, 2).

• XR → useful if you suspect an acute injury/trauma (e.g., avulsion, fracture). Less sensitive in overuse without trauma (3).

• CT → rarely ordered by first-contact clinicians; usually reserved for orthopaedic/paediatric specialists, particularly for surgical planning (4).

Lateral Elbow: Compression Problems

Panner’s disease (osteochondrosis of the capitellum)

• Who: Boys typically <10 years (1, 5).

• Clues: Weeks of lateral pain, stiffness, possible flexion contracture, small effusion (6).

• Imaging:

  • MRI preferred — marrow changes, necrosis, fragmentation.

  • XR may show capitellar flattening/fragmentation but can miss early disease (7).

• Prognosis: Self-limiting; rest and activity modification. Excellent outcomes (5).

  

Capitellar OCD (osteochondritis dissecans)

• Who: Adolescents 11–15+ years (1, 5).

• Clues: Lateral pain, loss of extension, catching/locking → unstable lesion or loose body (6).

• Imaging:

  • MRI gold standard for staging stability (4).

  • XR useful starting point, but often normal early (3).

  • CT for surgical planning if instability or loose bodies confirmed (8).

• Prognosis: Stable lesions may heal with prolonged rest (up to 6 months). Unstable lesions and loose bodies → surgical management.

Posterior Elbow: Shear Problems

Olecranon apophysitis / persistent physis

• Who: Adolescents 12–16 years; physis normally closes ~14–16 (7, 9).

• Clues: Posterior pain with resisted extension; tenderness at olecranon (2).

• Imaging:

  • MRI best for subtle physeal stress reactions and marrow edema (6).

  • XR if acute injury suspected — look for apophyseal widening or fragmentation (9).

  • CT only at specialist level if displaced or non-healing (4).

• Prognosis: Most settle with rest and activity modification. Surgery if displaced or persistent non-union (5).

  

Posterior Elbow Impingement/Ulnohumeral Joint Effusion

• Who: Throwers, gymnasts (1).

• Clues: Pain at terminal extension, loss of extension, mechanical catching/locking (7).

• Imaging:

  • MRI to assess cartilage, synovitis, loose bodies (4).

  • XR to detect posterior spurs or loose bodies (9).

  • CT reserved for surgical planning.

• Prognosis: Activity modification if mild; arthroscopy if symptomatic with mechanical block (6).

Anterior Elbow: The Rare Zone

Anterior overuse pathology is uncommon in kids.

• Clues: If pain localises anteriorly, think intra-articular irritation, loose body, or radiocapitellar overload rather than tendon.

• Imaging:

  • MRI if XR is normal but pain persists (8).

  • XR only if acute trauma suspected.

  • CT almost never first-line.

Differential Diagnosis: Don’t Forget What Can Refer to the Elbow

Just as paediatric hips can refer pain into the knee, clinicians should remember that paediatric shoulders and upper arms (humeri) can refer pain distally around the elbow. Not all “elbow pain” originates at the elbow. Be mindful of:

• Little Leaguer’s Shoulder — a proximal humeral epiphysis stress injury seen in throwing athletes. These kids may report vague arm or elbow discomfort rather than true shoulder pain.

• Distal humeral bone stress injuries — particularly in high-volume throwers, tennis players, or athletes with rapid spikes in loading. Early symptoms can masquerade as nonspecific elbow pain, especially posterolaterally.

If local examination of the elbow doesn’t match the severity of symptoms, or if pain is reproduced with shoulder loading, torsion, or axial stress through the humerus, expand your assessment proximally. The skeletally immature arm often distributes stress across multiple growing centers — and missing the real source can prolong the condition considerably.

Don’t Forget the Younger Fractures

Even though this blog focuses on 10+ athletic kids and overuse injuries, clinicians should still keep key paediatric fracture patterns in mind:

Lateral Condyle Fractures (≈4–10 yrs)

• One of the most commonly missed elbow fractures (DeFroda 2017).

• May present as simple lateral elbow pain with minimal swelling.

• If the story doesn’t fit clean overuse → get an XR.

Monteggia Fractures (≈4–10 yrs)

• Not an overuse injury but mentioned here for interests sake (as a Parent myself)

• Any ulnar injury should prompt a check for radial head dislocation.

• Kids may only describe vague elbow or forearm pain.

  

Rule of thumb:
If the symptoms, mechanism, or irritability don’t behave like an overuse pattern — think fractures first - not middle aged pathologies (tendinopathies, tennis elbow, golfers elbow etc).

Summary

The paediatric elbow isn’t a smaller adult elbow. Its weak points are different.

• Anchors (apophyses) (where ligaments and tendons attach)

• Foundations (bone)

• Growth plates (physes)

So if an athletic child has persistent elbow pain, don’t default to “tennis elbow.”
Look instead for Panner’s, OCD, olecranon apophysitis, or posterior impingement.

Final Word for Parents

If your athletic child has ongoing elbow pain that isn’t improving — especially if they’ve already seen a physiotherapist or provider who usually treats adults — please don’t stop there.
See an experienced healthcare provider with extra training and experience in athletic paediatrics. These injuries need the right eyes, at the right time.

References

1. Hutchinson MR, Ireland ML. Overuse and throwing injuries in the skeletally immature athlete. Instructional Course Lectures-American Academy of Orthopaedic Surgeons. 2003;52:25-36.

2. Migliaccio D, Wang NE. Common Pediatric Upper Extremity Overuse Injuries. Pediatric Emergency Medicine Reports. 2017;22(1).

3. DeFroda SF, Hansen H, Gil JA, Hawari AH, Cruz Jr AI. Radiographic evaluation of common pediatric elbow injuries. Orthopedic reviews. 2017;9(1):7030.

4. Nocerino EA, Cucchi D, Arrigoni P, Brioschi M, Fusi C, Genovese EA, et al. Acute and overuse elbow trauma: radio-orthopaedics overview. Acta Bio Medica: Atenei Parmensis. 2018;89(Suppl 1):124.

5. Greiwe RM, Saifi C, Ahmad CS. Pediatric sports elbow injuries. Clinics in sports medicine. 2010;29(4):677-703.

6. Hennrikus WL. Elbow disorders in the young athlete. Operative Techniques in Sports Medicine. 2006;14(3):165-72.

7. Crowther M. Elbow pain in pediatrics. Current reviews in musculoskeletal medicine. 2009;2(2):83-7.

8. Andelman S, DiPrinzio E, Hausman M. Elbow injuries in the pediatric athlete. Annals of Joint. 2018;3(3).

9. Hill CE, Cooke S. Common paediatric elbow injuries. The open orthopaedics journal. 2017;11:1380.

Need help or a second opinion?
If your child is active and experiencing ongoing elbow pain, don’t wait for it to “grow out.” These conditions can be accurately assessed through telehealth/video consultations as well as face-to-face appointments. Whether you’re in Canberra or the surrounding region, I’m only one step away. It can be difficult to find a Musculoskeletal Healthcare Professional with specific training and experience in paediatric conditions affecting young athletes — but that’s exactly the space I work in.

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Before we dive in, a note: this case is shared with full patient consent, including pictures of their ‘loose bodies’ extracted from their elbow during the operation which I had the privilege of observing. Thanks also to the Surgeon, their team, and the theatre staff for having me.

Some elbows age quietly.
Others age like a dial-up modem exposed to a Canberra winter — slow, stiff, and one small stress away from complete meltdown.

This is a story about the second kind.

The Case: The Bent, Grumpy Elbow That Wouldn’t Behave

A 50–60-year-old very active and adventurous gent came to see me with a non-dominant elbow that had recently gone from “stiff but fine” to “I can’t even touch my face”.

As always, 90% of the public (and half the health system) default to calling any elbow pain “tennis elbow”. But this clearly wasn’t that.

Important bits:

• Old fracture decades ago → radial head + capitellum involvement.

• Always been a bit stiff, but not symptomatic.

• Suddenly:

  • Loss of extension (first sign)

  • Then loss of flexion (couldn’t touch his face easily)

  • Grip strength painful but not convincingly lateral tendinopathy (grip painful… but strong)

  • Achy inflammatory pattern, worse later in the day, often at night

  • Global elbow pain … posterior, laterally, and inevitably anterior… which is clinically when you know things are “pretty far gone” if it isn’t a distal biceps tendon issue.

So the patient had a moderate elbow case of “Und Hier Syndrome”.

Every part of the story so far pointed at a joint-driven, not tendon-driven, pathology.

So my clinical picture was screaming: “the joint is cranky and inflamed” (capsular inflammation/synovitis)

From here on, I may (or may not) have leaned far too heavily on references to a very famous adventure-movie hero. My team of entirely hypothetical lawyers has strongly advised that, to avoid attracting the attention of one of the world’s biggest movie studios (let’s just call them Dalt Wisney), I should make things obviously, unequivocally different.

So allow me to introduce the Healthcare Warrior who lives rent-free in my mind:

Doctor Montana Joans.

Because an adventurer-type patient absolutely deserves an adventurer-type narrative.

Dr Joans is part Clinician (in the early stages of this case), and part Surgeon (in the latter stages… when it’s very clearly not the Physio holding the scalpel… natürlich).

However before we commence our short but epic clinical journey, I’d like to acquaint you with what a calm joint looks like in my mind (and also on the arthroscopic camera):

und jetzt… here is what a Cranky and Inflamed joint looks like:

Initial Management: Anti-inflammatory

We trialled:

• 2–4 weeks anti-inflammatories

• Cutting out all weight-bearing (“avoid push-ups”) and loaded extension (“avoid tricep dips type movements”)

• Eliminating other aggravators (eg: boxing, planks, push-ups)

• Monitoring Range of Motion (ROM) + grip strength

  • Functional ROM (“can you touch your face yet?”) as well as ROM objective measures.

  • Grip Strength utilising a Handheld Dynamometer

    

He improved, but only partially.
Then… regressed again with very little provocation.

That’s the thing with a truly cranky joint:
Push it, and it pushes back harder. Nicht sehr gut!

Diagnostic Imaging: Lots of Smoke, No Clear Fire

Given the traumatic history (radial head and capitellum impaction fracture), XR referral was first, followed by an MRI shortly after.

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The Two Cohorts: Who’s Sitting in Front of You?

When it comes to managing meniscus tears, the clinical pathway shifts depending on who’s sitting across from you. In general, we’re dealing with two main groups.

The Young and Wobbly

Adolescents to early 30s. Usually sporty. Often explosive movers. Almost always “knee incident” stories that involve a twist, pivot, tackle, or some flavour of high-force trauma. MRIs are more common, earlier, in this cohort.

Meniscus tears matters more with these young folks. These aren’t slow degenerative changes marinating over decades. These are clean, traumatic hits — and if you miss the mark on managing them, you could be lining them up for early-onset osteoarthritis or a joint surface that’ll age like milk, not wine.

The aim here is clear: preserve as much meniscus and articular cartilage as you can. Rehab will need to be longer and smarter. If they go under the knife, they’re more likely to get a meniscus repair.

The Old and Stiff

Ah yes — the 40ish+ crowd. Our weekend warriors. Our Masters comp legends.

These knees have stories. Workload. Life load. Sport load. Maybe too many squats. Maybe none at all. And look — I know calling them old and stiff sounds harsh. But I say it with love. I’m one of them. I go to the Club Meetings (1^st Monday of Month at the local Scout Hall).

What matters here is that the rules change. The tissue healing window isn’t the same. The activity goals are often simpler — walk a few Ks, chase a toddler, squat to tie a shoe without grimacing. The risk-benefit ratio on surgery is completely different.

And sure, sometimes there is a real traumatic event — a fall, twist, or dodgy step that flipped the joint into chaos. But again: same label, different plan.

If they end up in theatre, it’s usually for a partial meniscectomy — snipping out the troublemaker.

Before we get to the Research – Something Super Important

Nothing gets an MSK nerd’s heart fluttering like a solid Trial Title Acronym.
So let’s kick things off with a quick quiz:

For each of these Titles below, are they a Taylor Swift Album or Meniscus Trial?

SO what do the Academic Boffins Tell Us

The research is now clear—and has been for years. Here’s but a sprinkle of research pixie dust:

• Meng et al. (2018) — Meniscus tears show up on MRIs in pain-free people. Structure ≠ symptoms (1).

• Stensrud, Roos, & Risberg — 12 weeks of exercise improved pain, function, and strength — without a single surgery (2).

• Kise et al. — In middle-aged patients without radiographic OA, supervised rehab matched surgery for patient outcomes — and beat it for strength gains (3).

• Herrlin et al. — Even in 2007, patients with degenerative tears and mild OA did just as well with exercise as with surgery + exercise (4).

Behold: the Peer-Reviewed Pixie Dust Edition — guaranteed to boost N values and placebo effects by 30%

“Alright Nick… but what about the Swifty trivia?”
Glad you asked.

How’d you go?

Did I trick you by dropping the extra “R” from STARR? If your RCT doesn’t have a catchy name, is it even real?

Alright, game faces off. Let’s get clinical and go to the Big Trials where researchers worked hard to produce high quality acronyms for their titles:

The TRIALs (Targeted Research In Arthroscopy & Loading)

Clinical Application

You’re not “delaying the inevitable” with rehab. You’re giving the joint a legitimate shot at recovery.

Caveat: When the Research Doesn’t Apply

The DREAM and STAR trials showed that supervised rehab often matches surgery — but only in the right knee.

Locked knees, big extension losses, unstable joints, or obvious mechanical symptoms? Those patients were excluded.

Even so, the DREAM trial’s secondary analysis (7) gave us a helpful nugget:

• Surgery was better for persistent mechanical symptoms like catching or clicking.

• But for pain, function, and quality of life? Rehab held up just as well.

So yes — rehab is powerful. But it’s not magic.

If a knee keeps clunking mid-squat, won’t get past 20° extension, or won’t calm down after 6–12 weeks of proper rehab — that’s not a rehab fail. That’s your sign to escalate.

But what are we looking for exactly?

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The Series:

• Prologue | A Clinician’s Flight Plan for MSK Care

• Chapter I | Neck and Low Back Pain

• (You are here) Chapter II | The Older Shoulder

Take-Off

Ensure you have completed all pre-flight checks, all patient baggage has been checked in and stowed, patients have been through all checkpoints, and have been thoroughly screened to ensure they are on the right flight.

Triage for Red Flags and Urgent Referrals

• If insidious/low force onset:

  • Continue without imaging initially for Musculoskeletal (MSK) presentations.

  • See a MSK clinician with a minimum of 45 minutes for the initial appointment.

  • XR if ruling out medical red flags.

  • GPs should refer to a reliable physiotherapist for low-cost/high-value care.

• If high force trauma history:

  • Immediate XR (usually done in ED/A&E) if severe pain or loss of glenohumeral joint (GHJ) function.

  • Follow up CT if fractures on XR and surgical referral is likely (most likely referred by orthopaedic specialist).

  • MRI if no improvement in GHJ function and pain despite rehab at weeks 6-8.

Patient History/Profile

• Classify the Patient into a Cohort:

  • To aid short-list of likely differential diagnoses.

  • Paediatric patients and young adults get different insidious onset and traumatic GHJ pathology than middle aged and older adults.

  • Females 50-60yrs are more likely to develop adhesive capsulitis.

  • Patients > 75-80yrs are less likely to have primary rotator cuff referred pain if it its their first presentation - check cervical spine.

• Inflammatory profile and metabolic status: Consider medical status (diabetes, obesity, smoker, menopause, auto-immune inflammatory diseases etc.)

• Psychosocial profile: Check for nocebic beliefs, especially those influenced by past healthcare providers and radiology, family history, patient goals, occupation, etc.

• Current medications: Review the list for unreported medical history.

• Previous prescription of oral NSAIDs: Assess tolerance and side-effects.

• Previous imaging and procedures: Review past imaging to rule out significant issues and check for effectiveness of recent US guided HCLA injections for Bursitis.

Patient History

• Mechanism of Injury: Hunt for the exact mechanism of injury. If insidious onset, query the 1-2 weeks in the lead-up to the pain

• Injury History: Have they had this before? What made it better/worse, what was the duration of symptoms back then?

• Pain Patterns for Differential Diagnostics:

  • Location Map out exact pain referral patterns “point with your finger where your pain is” – pain past elbow, or pain into shoulder blade less likely to be Glenohumeral Joint.

  • Irritability/Severity – Mild/Moderate/Severe – speaks to the sensitivity of different structures

  • Pain Onset - Mechanical onset when using shoulder, or is it an achy pain after upper limb tasks.

  • Daily Pattern - Is there pain at night and in what positions (or is it any position?)

• Top 3 painful tasks/activities – Track the top 3 things that bother the patient. (Utilise the PFPS formally or use it as a guide for tracking)

Physical Examination

• Clear Cervical Spine as Cause/Contributor:

  • Glenohumeral joint and Cervical Spine are both relatively easy to rule out with good assessment.

  • Pain location (knowing what refers where) helps significantly here.

  • Bilaterality (pain on both sides) usually suggests Cervical Spine referral moreso than both GHJs.

  • Cervical Spine Cluster test: Upper Limb Neural Tension Tests, Spurlings Test, Specific Palpation of cervical column.

  • If suspected, utilise Neck and Low Back Pain Checklist

    

• Rule out Adhesive Capsulitis/Frozen Shoulder – pain > stiff phase or stiff > pain phse. Loss of ROM in >2 directions and highly irritable.

• Clear Other Shoulder Joints – Acromioclavicular Joint (ACJ) and Sternoclavicular Joint (SCJ)

• Medical causes for pain: Obtain a solid medical history to rule out visceral pain referral and other medical causes (infections, neoplasms, insufficiency fractures).

• ROM, Strength and Functional Capacity Testing

  • AROM: Flexion, Abduction, External Rotation, Internal Rotation

    • PROM past the first point of AROM pain to rule out contractile tissue pain inputs.

      • A significant restriction in 2 or more ROM directions, particularly ER would suggest frozen shoulder or another significant ROM restricting pathology.

  • IR+ER ROM (Total ROM (TROM)) in Supine

    

  • Observation – for loss of muscle bulk (eg: infraspinatus muscle), check for pop-eye sign (bicep bunching), observe quality of ROM movement

  • Isometric Strength – utilising fixed or handheld dynamometry

    • External Rotation (0deg abduction) (ER0)

    • Internal Rotation (0deg abduction) (IR0)

    • External Rotation (90deg abduction) (ER90) - If ROM >110deg and patient usually active above shoulder height with gym, exercise, sports, ADLs, and/ or occupation.

• • If good enough strength with IR0/ER0 and pain-free ROM > 135, consider ASH Test on force plates, fixed dynamometry or simple bathroom scales.

  • Apprehension test in upright position or supine if instability is suspected (less likely in the older shoulder)

• • Palpation

    • Cervical spine (Csp): Palpation is reliably sensitive but not specific (can be painful in asymptomatic patients), but absence of pain on palpation usually makes cervical spine issues less likely. There is a skill to correctly palpating the cervical spine with the patient in supine and head turned away, find an experienced practitioner to show you how.

    • Shoulder: Palpation of GHJ is unreliable (doesn’t rule in or out), not sensitive and not specific. Palpation of ACJ and SCJ reliably specific and sensitive (easy to rule out with palpation). Palpation of long-head biceps tendon (LHB) is unreliable for specificity, but reliable for sensitivity (absence of pain in bicipital groove makes LHB pathology less likely – if LBH is still there).

Diagnostic Labels to help guide management:

• Pain levels: Label as mild/moderate/severe; avoid dwelling on VRS (“1-10 scale”).

• If Cervical Spine involved, see Diagnostic Labels in Neck/Low Back checklist

• Rotator Cuff Referred Pain for weak and painful shoulders.

• Shoulder Instability for unstable and painful shoulders.

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The Series:

• (You are here) Prologue | A Clinician’s Flight Plan for MSK Care

• Chapter I | Neck and Low Back Pain

• Chapter II | The Older Shoulder

  (future chapters not in order)

• Future Chapter | Patellofemoral Pain

• Future Chapter | Lateral Elbow Tendinopathy (Tennis Elbow)

• Future Chapter | Ulnar sided wrist pain

• Future Chapter | Hip Joint Pain

• Future Chapter | Achilles Rupture Non-Surgical Pathway

• Future Chapter | Knee ACL Rupture Non-Surgical Pathway

• Future Chapter | Plantar Fasciopathy

From Barrel Rolls to Smooth Landings: A Lesson in Broad Perspective

Many moons ago, in a land far far away, I was flying Plastic Parrots (CT-4 Airtrainer) and Mudry CAP-10 aircraft through the skies above Tamworth, NSW, Australia.

Performing barrel rolls, loop the loops and spin recovery training as part of Basic Flight Training School (BFTS) for the Australian Defence Force.

If you haven’t noticed, I’m not a pilot, therefore you’d guess things mustn’t have gone well — which is a good guess.

Turns out I could take off fine, buzz around upside down and inside out, recover from a stall and spin, but for the life of me: I could not land.

No matter how hard I concentrated, every approach ended the same: BUMP, BUMP, BUMP. Under-carriages were not my friend. It wasn’t until a chat with my brother (airline pilot) and cousin (pilot and ATC) that I realised what I was doing wrong.

I was locked onto the tarmac just in front of my nose — the small picture — which led to jerky, erratic corrections. What I needed was to look further up the runway — the big picture — and make calm, subtle adjustments that would eventually bring me in smooth.

Why use Checklists?

Clinical practice is no different. If we fixate only on the immediate pain in front of us, we miss the broader flight path. The patient’s history, psychosocial load, long-term goals, and functional destination all matter.

Aviation, surgery, and construction all use checklists to reduce error in complex, high-risk environments.

Healthcare should be no different. A structured checklist doesn’t replace experience or conversation — it anchors it. It keeps us from missing the fundamentals that matter most.

What These Checklists Are — And What They’re Not

This series isn’t about handing clinicians a recipe book. Musculoskeletal care isn’t cake-baking, patients aren’t sponge cakes, and they also don’t fit neatly into cookie-cutters.

Each chapter in the Take-off to Touchdown Series will have its own checklist, designed as a troubleshooting tool for when the flight isn’t going to plan — when symptoms flare, when progress stalls, when smoke starts coming into the cabin.

These checklists are not scripts. This is not “Checklistology.”

I don’t sit with a clipboard, ticking boxes while the patient tells their story. Think more like a police investigator interviewing a neighbourhood. The structure runs in the background, but the conversation stays human, fluid, and story-driven.

These checklists don’t replace sound reasoning, nuanced conversations, or condition-specific skills. They’re here to make sure that in the chaos of turbulence, the most important steps aren’t missed.

It’s a structured safety net — a way of zooming out to see the big picture, while still allowing clinicians to fly the plane their own way.

The Flight Plan

Across this series, I’ll use a pilot’s checklist as a metaphor for injury management.

Each condition will get its own version — but the flight stages remain the same:

• Take-off → gathering history, screening, and first impressions.

• Cruise → the rehabilitation journey: sometimes short and smooth, sometimes long with detours.

  • Turbulence → when symptoms flare, when further investigations are needed, or medical management enters the cockpit.

• Landing → return to work, sport, and life.

  • Emergency Landing → when the flight diverts: surgical referral, red-flag escalation, or alternate care.

    

This prologue was your flight briefing.

Please now fasten your seatbelts, set your tray tables to the upright position, and make sure your window shades are up — we’re cleared for take-off.

The Series:

• (You are here) Prologue | A Clinician’s Flight Plan for MSK Care

• Chapter I | Neck and Low Back Pain

• Chapter II | The Older Shoulder

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Note: This blog is an adjunct piece to my upcoming blog:
✈️ Takeoff to Touchdown | Managing the Older Shoulder
(Check back soon for the link once it’s published.)\

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Scenario

It’s spring in Australia.

A 40–60-year-old walks into your clinic with an ultrasound report in hand and the classic line:

“I’ve got bursitis. The GP sent me for some physio.”

They’ve had a dull ache in the shoulder for weeks. The pain is non-mechanical, there throughout the range, and strength is down about 20% (as it almost always is in painful shoulders). They didn’t “earn” bursitis with an overhead workload — it’s just a shoulder that started nagging after some weekend gardening and hedge trimming.

They’ve already had one US-guided corticosteroid injection — $285 billed after Medicare chipped in $120. It did nothing. Now they’re lining up for another.

You assess them properly. Turns out, the shoulder joint itself is fine. The pain is referred from the cervical spine.

So… how did we get here?

What the Bursa Is — and Isn’t

A bursa is a synovial-lined sac filled with a small amount of viscous fluid. It serves as a biomechanical buffer between structures that would otherwise rub — e.g., tendon against bone, tendon against tendon, or skin against bone.

The subacromial-subdeltoid (SASD) bursa is not a troublemaker by default. Its job is to glide and cushion between the cuff, deltoid, and acromion during abduction. Yes, it “contacts” the acromion above ~80° — because that’s its normal role (Ivanoski 2019; Ruangchaijatuporn 2017).

It can thicken with repetitive load, much like a callus on your hand. That’s adaptation, not pathology. It’s only when it becomes oedematous, inflamed, or sensitised that it becomes a pain generator.

And we don’t just have one, there are 5-6 bursae commonly described, but we can have up to 8-12 in and around the glenohumeral joint.

Why Ultrasound Over-Diagnoses Bursitis

Ultrasound reports often highlight “thickened bursa” or “impingement with abduction” as if these equal pain. They don’t.

• Structural changes are common in asymptomatic shoulders. Subacromial bursal abnormalities appear in up to 90% of pain-free adults (Ibounig 2025; Gill 2014; Maronin 2017; Girish 2012).

• Dynamic contact isn’t pathology. The bursa is supposed to glide and compress under the acromion. Calling that “impingement” is like reporting that knees “impinge” when squatting.

• Bursal effusion and enhancement aren’t specific. Older sonography linked effusion with cuff tears (Hollister 1995), and contrast MRI showed enhancement in both painful and painless cuff tears (Hodgson 2012). In other words, imaging doesn’t tell you where the pain is coming from.

  

So when we see reports of “bursitis,” what we often have is a structural finding with no proven link to the patient’s pain.

What Real Bursitis Looks Like

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⚠️ Content Warning
This blog contains cadaveric images shown for anatomy learning purposes. These images are used in an educational context to help illustrate musculoskeletal structures. Please proceed with awareness if you may find such material distressing.

If you’ve read my companion piece — Takeoff to Touchdown | Managing the Older Shoulder — you’ll know the older shoulder is full of paradoxes. Some patients with massive tears keep functioning, while others collapse after what looks like a “tiny nick” on MRI.

This blog digs into the hidden reason: the rotator cuff cable - the suspension bridge wire helping distribute load across the important rotator cuff insertion.

Spoiler — it’s not about the size of the tear, it’s about whether the suspension bridge wires are still holding.

What Is the Cable (and the Crescent)?

Back in 1993, Stephen Burkhart introduced the world to the shoulder’s “suspension bridge” (1).

And like any good metaphor, once you’ve heard it, you can’t unsee it.

• The cable → a thick, transverse band of fibres running across the cuff, acting like the load-bearing suspension wire.

• The crescent → a thinner, more fragile lateral insertion, prone to tearing but less structurally important.

  

So when the crescent tears but the cable stays intact, patients can sometimes shrug and carry on.

But if the cable itself is disrupted? Even a “postage stamp” tear can cause major loss of strength and control (2, 3).

Why Does It Matter Clinically?

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Let’s get one thing straight right off the bat:
Kids. Are. Not. Little. Adults.

Say it again. Especially if you've ever diagnosed a 9-year-old with an adult-style meniscus tear or handed out a generic patellofemoral pain label for an acute knee injury that happened in PE class.

Because paediatric knees don’t just scale down adult anatomy — they behave differently, fail differently, and need to be assessed differently. Misunderstand this, and you’re locking a kid in a Zimmer splint for 6 weeks when they needed 2 weeks of movement, or missing a tibial spine avulsion while looking for a torn ACL.

Before we dive into red flags, imaging, and rehab decisions — let’s quickly spell out why the paediatric knee plays by a different rulebook.

Paediatric Knee Injuries Are Not Adult Knee Injuries

Let’s review what the research says:

🔹 Kids don’t rupture ligaments easily — they avulse.
In children, the physis is the weak point — leading to tibial spine avulsions instead of ligament tears. (1)

🔹 Partial ACL tears on MRI are usually complete.
In their series, 99% of “partial” tears were complete at surgery, and the ACL may appear thin in normal kids — don’t be fooled by the scan​.

🔹 Meniscal injuries are often delayed and secondary.
Tears like ramp lesions or bucket handles often appear later, not at time of injury. You may miss them on early MRI but find them at week 6 when instability continues. (1, 2)

🔹 Bone injuries > soft tissue.
You’ll see more bone bruises, condylar impaction, tibial plateau irregularities, and growth plate complications than ligament ruptures — many of which can guide care, even if they don’t require surgery. (2-4)

Translation?
Using adult MRI criteria, adult diagnostic flowcharts, and adult expectations leads to misdiagnosis, mismanagement, or over-treatment in kids. (5)

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People like a chat with someone friendly, with charisma. They also like a clinic that looks like a clinic.

A white coat. A polished reception area. A provider with a logo, a script, and a gentle nod as they tell a “scientific-sounding” story about why this one specific intervention works perfectly — for this injury, at this time, in this patient.

But you step back and realise:
That exact same story was told to everyone last week.
Different symptoms, same narrative. Different region, same hammer.

That’s not healthcare. That’s branding.

It’s the equivalent of Lyle Lanley - aka The Monorail Guy from the classic (and now very old… like me) episode of The Simpsons.

For all of those readers born from 1995 onwards, just auto-replace all future Monorail Guy references with Belle Gibson or The Apple Cider Messiah.

Contextual Effects 101

Contextual effects are the non-specific benefits that come from the experience surrounding the intervention — not the intervention itself.

Things like:

• The clinical setting

• The confidence of the provider

• The trust the patient feels

• The “plausible science-y” explanation given

• The therapeutic ritual

• The sing song in the community hall

And yes — these can have short-term value.
But when these replace good healthcare, we’re in trouble.

Ask yourself:
If the exact same treatment were delivered to me at a bus stop by a stranger — would it still work?
If not, what are we actually treating?

Monorail Thinking

Everything works beautifully — until it doesn’t.
Patients go around and around in that comfortable monorail loop of passive care, short-term analgesia, charisma, and contextual sugar.

And then the symptoms worsen. Or change. Or they fall off the track.

And now it’s our mess to clean up. And that clean up takes longer than it should, and usually costs more too.

Real-World Monorails

• A patient with cervical radicular pain spends two years having weekly adjustments and unnecessary spinal imaging.
  Nothing was “subluxed.”

  The problem wasn’t “malalignment” — it was persistent inflammation.
  Two weeks of oral NSAIDs, stop the frequent shopping-mall massages on it, reduced sedentary time at work, and a progressive walking program?
  Gone. Completely.

• A patient with “tennis elbow” receives fortnightly dry needling under workers’ compensation for over a year. Then it started in the other arm. Then it turned into “RSI in both arms”.
  The source? C6 foraminal stenosis.
  The cause? Undiagnosed ankylosing spondylitis.
  No one looked past the elbow. No one asked the systemic questions.

• A patient with “sciatica” receives cupping and toxin talk for months.
  The true cause? A growing S1 nerve root compressive cyst.
  Whoopsy, probably should have ordered that MRI sooner - except they saw a soft-tissue therapist (who the patient thought was a physiotherapist - because they look and sound the same except one has been trained to look for red flags and can refer for imaging).

Extreme examples? Sounds like it…. but no, it’s daily stuff.

And the more we shrug off the damage of low-value care, the more these become someone else’s patient to rescue.

Palliative ≠ Pointless, But Label It

There’s a place for feel-good care — when it’s honestly labelled.
If the goal is comfort, relief, stress reduction — that’s fine. Just don’t sell it as treatment.
Don’t tell patients that hickeys from a suction cup are detoxifying fascia.
Don’t tell them a needle in their glute is realigning their spine.

If you’re in the business of feeling better, label it as feel-good care.
Don’t pretend it’s fixing the cause.

Is it a Do Good, or just a Feel Good. Feel Goods are great, but call them what they are.

The Safety Net and the Circus

In this system, some of us are the safety net.

Others are riding tricycles around the edge in clown shoes, tooting their own horns about posture, energy flow, or magical spinal resets.

When things go bad, those of us in the net are expected to:

• Diagnose what others missed

• Reverse years of false beliefs

• Win back patient trust

• Deliver hard truths

• Do it all in under 30 minutes

Catch a patient early, and the rehab is efficient, empowering, and short-lived.
Catch a patient after a decade in the woods, and it becomes:

• Slow

• Costly

• Emotionally draining

• Narratively fragile

Changing someone’s pain is easy.
Change their belief system?
That’s the real work.

BOO Therapy and Hug Therapy

If you want a temporary analgesic effect, just scare someone.
Literally.

Sneak up behind them and yell BOO!

Their adrenal glands will trigger a full fight-or-flight response:

• Catecholamine release (adrenaline, noradrenaline)

• Increased HR and BP

• Dilated pupils and bronchi

• Peripheral vasoconstriction

• Endogenous opioid release

Pain = dulled.

Or go the other way: give them a hug.

A trusted touch can release:

• Oxytocin

• Dopamine

• Serotonin

• Endorphins

All the same ingredients that make low-quality care feel therapeutic.

So where’s the clinic offering BOO Therapy or Hug Therapy?
They’d probably be safer than dry needling or neck cracking.

This Isn’t Profession Bashing

This isn’t about “chiro bad, physio good.”
Some chiropractors are outperforming physios.
Some osteos are ahead of orthopaedic specialists.
Some GPs are 15 years behind in managing low back pain.

It’s not the profession.
It’s the thinking.
And the systems that allow thinking to go unchecked.

It’s the Modality Therapists - the One Tool Providers (eg: The ‘Dry Needling Physio’, where the Needle is always the answer).

Final Word

Contextual effects are real.
So are missed diagnoses.
So are narrative traps.
So are false beliefs that harden like scar tissue around a patient’s identity.

It’s not enough for something to feel good.
It has to do good.
It has to help someone get off the monorail — not ride it until the track ends in fire.

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"It’s just an ankle sprain."

They limp in at week three. Or week five.
The swelling’s still impressive. The story’s vague.

"It wasn’t too bad… at first."

And now they’re confused that it’s still sore and useless.

This is the classic lateral ankle sprain that wasn’t bad enough to get treated properly but now refuses to go away quietly. Sometimes they’re unlucky. Sometimes they’ve walked on it too long. Often they’ve never had imaging and are still trying to figure out if it’s “just a sprain” or “something worse.”

And that’s where we come in.

This blog is for the ankle that comes in late, swollen, and untreated, but still salvageable.

We're not talking high ankle sprains.
We’re not chasing medial deltoid ruptures.
This is your stock-standard, under-managed lateral ankle—a physiotherapy staple that still gets underestimated.

They Walk In (Barely). What Now?

Your job is to do what no one else has yet:
Assess, immobilise, and plan.

Start with the Ottawa Ankle Rules, which are dead simple but surprisingly underused:

✅ Order an x-ray if there is pain in the malleolar zone AND
🔸 Bone tenderness along the posterior edge or tip of the lateral or medial malleolus, OR
🔸 Inability to bear weight both immediately and in the clinic

✅ For midfoot injuries, x-ray if there is pain in the midfoot zone AND
🔸 Bone tenderness at the base of the 5th metatarsal or navicular, OR
🔸 Inability to bear weight

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There’s a common mistake many clinicians make early in their tendon-rehab journey—assuming all tendons behave the same.

They don’t.

We can’t keep copy-pasting lower limb protocols into upper limb presentations and expecting things to just "work." This is a nuanced game—one where understanding the job description of the tendon in question matters as much as the load dose itself.

I’ve seen the tendon bandwagons come and go:

• The Eccentrics fix all the Tendons phase.

• The Isometrics fix all the Tendons phase.

• The Isometrics then Heavy Slow Isotonics then Eccentrics then Plyometrics - fix all the Tendons phase.

This blog explores the key clinical differences between lower limb and upper limb tendons, why we treat them differently, and how failing to recognise the distinction can derail your rehab approach before it even begins.

Lower Limb Tendons: Load-Tolerant, Load-Thirsty

Think of the lower limb classics: the Achilles and Patellar Tendons.

Patellar tendons go vertical. Achilles tendons go horizontal.

Different angles, same story:

These are tendons that are designed to absorb and transmit massive loads, often on a daily basis. They thrive on load—so long as it’s progressive, measured, and dosed correctly.

They’re used to dealing with:

• Ground reaction forces from running, landing, and changing direction

• Rapid stretch–shortening cycles

• Bodyweight multiplied several times over during dynamic movement

In most cases, we’re dealing with tendons that respond predictably to:

• Heavy Resistance (Heavy Isometric and Isotonic gym tasks. And let’s be clear: "Heavy Resistance" isn't a blue resistance band. We're talking 1.5 to 3 times body weight in some instances.)

• Progressive energy storage and release work

• Clearly defined return-to-sport markers (e.g. hop tests, SL calf raises, etc.)

Pain during loading is often permissible—if it’s controlled. We have enough data and clinical experience to guide patients through tolerable pain with confidence. “Some pain is okay” is a phrase that holds weight in lower limb rehab. In fact, sometimes it’s essential to get the job done.

Please…. if you think a patient in front of you has Patella Tendinopathy and they aren’t an elite jumping athlete, make sure you rule out other differential diagnoses as this rarely occurs in other cohorts and is commonly misdiagnosed.

Not All Tendons Are Built for Bounce

Here’s a useful lens I’ve found helpful—and clinically clarifying:

Some tendons are Springs. Some are Stabilising Straps.

That’s not textbook terminology, but it holds up well in practice. More formally:

• Stretch–Shortening Cycle (SSC) tendons are built to absorb load, store it, and release it.
  Think Achilles, Patellar, and yes—even the Common Wrist Flexors when acting as prime movers.
  These tendons are built for propulsion. They behave like biological springs—compressing, recoiling, and repeating with each movement cycle.

  

• Then we have Positional (or Postural) Tendons—the ones that exist to stabilise and optimise joint positioning.
  Think Gluteal tendons, Common Wrist Extensors, and the Rotator Cuff.
  Their job isn’t force production—it’s coordination, precision, and positional control.

This distinction fundamentally changes our rehab approach.

With SSC tendons, we’re building up tolerance to load and stretch—encouraging them to store and release energy efficiently.
With positional tendons, we’re often trying to reduce sustained compression, improve joint mechanics, and retrain how the tendon holds its post while the limb moves around it.

That’s why most of us no longer prescribe loaded wrist extensions for lateral elbow pain. Instead, we favour positional exercises—like holding a weight in a specific wrist position while moving the shoulder or elbow through functional tasks. The tendon doesn’t need concentric overload. It needs support. Coordination. Re-integration.

These Tendons Tell Bigger Stories

What’s even more interesting—and clinically revealing—is that it’s often these positional tendons and complexes that act as barometers for the system.

They’re the ones that don’t just get grumpy from a heavy lift or a long day on the tools.
They become painful, stiff, and stubborn when the system itself is under pressure.

Think:

• Middle-aged patients with subacromial pain that lingers for months

• Chronic lateral elbow pain that came on “out of nowhere”

• Bilateral gluteal tendinopathy in someone with central adiposity and poor sleep

There’s often a metabolic backdrop here—insulin resistance, altered lipid profiles, low-grade systemic inflammation.
In women aged 50–60, menopause is another key player—bringing a reduction in collagen turnover and tendon healing capacity. This is a particularly common story in gluteal tendinopathy.

These tendons may not be failing due to excessive load… they’re failing to adapt because the systemic environment is hostile to repair.

Yes, sometimes these issues follow a clear overload event. A weekend gardening blitz. A sudden increase in tennis.
But more often, these are the tendons that take 6–12 months to settle—regardless of how evidence-based your exercise prescription is.

Check out the below Tennis Elbow update on how that plays out:

These cases require a broader rehab lens.
Rehab becomes less about tendinous capacity, and more about physiological readiness.
Less about sets and reps. More about managing the load above the neck and below the skin.

Upper Limb Tendons: Smaller, Fussier, and Far Less Forgiving

Enter the world of lateral elbow pain and rotator cuff overload—transitional tendons that sit somewhere between the worlds of load and control.

Let’s take the ECRB, the main driver of tennis elbow.

Unlike the Achilles, ECRB’s job isn’t propulsion. It’s postural—to hold the wrist stable during grip, type, lift, or repetitive fine motor tasks. It doesn’t love big concentric/eccentric cycles. It loves control.

And therein lies the difference. These tendons:

• Fail under compression far more often

• Live in low-load environments and then get overloaded by task repetition, awkward postures, or sudden demands (hello, first-time house painter with a roller)

Applying HSR to these tendons without thought leads to trouble. They often don’t tolerate pain. And the same tendon that flares with a TheraBand can be doing 8,000 reps of typing at work the same day.

Compression Is the Variable That Changes the Game

In lower limb rehab, we often embrace compressive positions in mid-late stage rehab.
Heel drop with dorsiflexion? Absolutely—perhaps not immediately, but inevitably.
Gluteal loading in deep hip flexion? Bring it on.

But upper limb tendons don’t play the same game.

• The radial head compresses the sensitised ECRB tendon when gripping in elbow extension and forearm pronation.

  

• The sensitised rotator cuff complex gets compressed in the sub-acromial space (which is their normal Monday-to-Friday job—but sometimes the sub-acromial space just needs a weekend or a two-week getaway).

  

• The proximal hamstring tendon (Runner’s Bum) gets compressed during hip flexion or by external surfaces like hard seating. Common in runners, deadlifters, and yoga practitioners, this tendon suffers a double-whammy of internal and external compression. It is especially prone to overload in middle-aged adults—particularly women in menopause—when stretching, sitting, or performing repetitive deep flexion activities. Rehab here means reducing compression, avoiding aggravating positions, and gradually reintroducing load via knee-dominant hamstring tasks before progressing to hip-dominant loading in neutral, then flexed positions.

  

• For these tendons, we often start by loading them out of compression (for Runners Bum, leg curls instead of hip hinges for example), then gradually build tolerance to loading into compressive positions. Ironically, those compressive positions are often the most efficient at generating force—calf raises in dorsiflexion being a perfect example. But we must earn the right to train there. It’s a phase-based approach, not a default starting point.

And sometimes, tendon overload is secondary—a result of something else in the kinetic chain breaking down.
Take the Achilles, for example. An older athlete might develop Achilles tendinopathy after a soleus injury. If the soleus fails to recover its force output, the Achilles can become overloaded by picking up the slack.
This is why we must assess surrounding muscle-tendon units—not just the sore spot.
Use dynamometry to confirm and quantify pain-free force production deficits, not guess them.

Clinical Takeaways

Here’s what we need to carry forward into our practice:

• Respect the difference in tendon purpose. ECRB ≠ Achilles. Rotator cuff ≠ patellar tendon. Function matters.

• Compression of sensitive tissues is often the villain in upper limb tendon pain. Load type (eg: positional) matters as much as load amount.

• Pain tolerance thresholds differ. “Push through a bit of pain” might help an achilles tendon —might flare a shoulder or gluteal tendon for a week.

• Sometimes it’s not the tendon—it’s a weak neighbour. Test it properly.

• Systemic load matters. Especially when rehab stalls, zoom out before doubling down.

Final Thoughts

Tendons are beautiful in their simplicity—until they aren’t.

In the lower limb, we often get away with cookie-cutter rehab plans. In the upper limb, we need nuance, patience, and a broader lens. The evidence base is catching up, but the clinical complexity has always been there.

So next time you catch yourself programming a wrist extensor the same way you’d load a quad, take a breath, pause, and ask:

What’s this tendon actually trying to tell me?

Sometimes, the answer isn’t in the sets and reps.
Sometimes, it’s in the story.

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Before we dive in, a note: this case is shared with full patient consent, including the use of their x-ray image. Many thanks to Her.

What follows is a straightforward case with a twist: a classic referral for low back pain that unravels into something completely different. We’ll walk through the key clues, the simple physical assessment that made it obvious, and the pivot point that helped get this patient onto the right path.

The Case That Walked Through the Door

She was in her late 60s, healthy, active, and still working as a professional — often travelling for work, juggling multiple legs across continents with a level of independence many envy: two major overseas walking holidays a year, navigating multiple stops with ease. A long-time walker by choice, not by obligation. She tried not to use her car. Her GP had referred her to me for "low back pain radiating to the left foot." A CT scan of the lumbar spine was already done and in hand.

That report, presented to me on arrival, stayed face-down on the desk.

I’ve learned to delay looking at imaging until I’ve listened. The goal isn’t to ignore scans, but to make sure they don’t hijack the clinical reasoning process before I’ve had a chance to form my own impression.

What followed was a familiar pain story. She described pain in both legs, but never in the classic posterior leg or buttock pattern we’d expect from a spinal radiculopathy. Instead, it was creeping down the lateral thigh, into the groin, and even to the lateral mid-shin.

Her worst side was the left, though it had started mildly years ago, peaked a month before our consult, and responded in the past to anti-inflammatories. Pain and spasms at night were prominent, and now even a 15-minute walk could elevate her symptoms to a 5/10.

At first glance, she looked like a classic candidate for the ‘spinal scan spiral’ — starting with a CT lumbar spine and possibly heading towards a spinal injection.

Clinical Reasoning, Not Default Pathways

This case highlights why thorough assessment matters more than inherited labels. As covered in my blog on differentiating lumbar, SIJ and hip pain, we need to stop assigning pain based on geography alone — especially when it’s continental geography. “Leg pain? Must be sciatica” is the mindset that gets people scanned, injected, and labelled.

We need to upgrade to cultural geography — the sort of mapping that recognises:

• SIJ pain can refer to the buttock or posterior thigh, but never to the foot

• Lumbar spine can go to the foot, but almost always tracks through the posterior chain

• Hip joint referral tends to hug the anterior thigh and groin, but can sneak all the way to the shin and foot

Physical Exam

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The first part of this post is an introductory preview—the valuable clinical insights, practical recommendations, and expert guidance are behind a paywall for paid subscribers only.

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If you find my free content helpful, becoming a paid subscriber gives you:
✅ Full access to expert-backed strategies and pain management insights
✅ Direct access to me via subscriber chat—ask me questions anytime
✅ Ongoing, high-value information normally provided in a clinic for hundreds of dollars

This post is a guide only and should not be taken as medical advice. It does not replace assessment and recommendations from a registered and regulated healthcare professional.

This blog is about recovery and load management — especially in tennis, where court surface, match volume, and S&C preparation all shape injury risk. Hard courts load the hips. Grass courts cook the hamstrings. Clay sits somewhere in between. Knowing how to manage transitions between surfaces, and how to condition athletes across a season, is key.

I explore that in more detail in this article on hybrid athlete load management:

For more on how surfaces impact injury and performance, see:

Initial Contact

“Nick, do you work weekends?”

I was contacted urgently by the father of a mid-adolescent male tennis player—a high-level state representative tennis player—who had just retired from a representative tournament match with hamstring pain. The parent believed it was a hamstring tear and was planning to see a GP for imaging.

I wanted to prevent the parent from getting unnecessary imaging (common), or the wrong imaging (also common), save costs, and more importantly, give the player a play vs no play assessment.

That’s why I offered to assess him on a Saturday morning, my day off — to nip that in the bud early, and besides: it's tennis. I can live, breathe, talk and play tennis all day every day.

Mechanism Notes & Medical Check

In the week leading up to the injury, the player had competed in 10 challenging matches across multiple formats, including Opens and U16s. During the third set of a match at the first tournament, he began experiencing left hamstring cramping. He pushed through, played the next match pain-free, and then reported a return of symptoms in the final — a tight, crampy sensation with difficulty straightening the leg.

Importantly, this sequence of tournaments also involved a surface change from hard court to grass. While hard courts typically load the hips more, grass courts place significantly more demand on the hamstrings—especially with lower bounce, greater need for lunging, and more deceleration from deeper court positions. Grass is a slow cooker for hamstring strain — lots of sliding and eccentric/isometric loading on the front leg, particularly when retrieving low balls. This shift likely compounded the fatigue and contributed to the overload pattern.

After just two days of rest, he travelled interstate for another tournament. In the first round, it was 6-6 in the first set of his first math, and whilst loading into a wide backhand, he felt a big stretch and “crampy pull” in the hamstring and had to retire from the match.

His family history included maternal hip dysplasia and Perthes disease, but his own medical history was otherwise unremarkable.

Assessment Findings (Day 4 Post-Injury)

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This post zooms in on acute lumbar spasm episodes—how to spot them, avoid overtreatment, and guide patients toward recovery without fuelling over-medicalisation. It complements the broader diagnostic framework in the main blog, with a special focus on contextual effects and systems thinking. Acute lumbar muscle spasms are a different beast entirely to your ‘standard Lumbopelvic +/- Lower Limb Pain’ (with a healthy dose of irony in that label).

They’re easy to spot: a well-localised, fist-sized patch of moderate-to-severe pain, often described as arriving “out of nowhere.”

Usually, the patient wasn’t even thinking about their back - they were thinking about the night routine for their 2 kids under 3yrs as they were pulling plates out of the dishwasher… and then BAM:

As always, we rule out the serious stuff first—neoplasms, fractures, infections, vascular causes—before we settle on the label: acute muscle spasm.

I explain this painful phenomenon to patients differently almost every time, however here’s roughly how the script goes:

“Your spinal system picked up on an irritant—usually in the neck or lower back—that wasn’t being addressed. And when you didn’t stop the irritant, your spine stopped you. My job is to make sure the irritant isn’t serious, and to help you recognise it next time—so your spine doesn’t have to pull the emergency brake again. The good news? The first time is usually the worst. What amplifies the pain is the panic—not understanding what’s happening, not feeling in control. Once you realise what’s going on, the fear drops. And when the fear drops, so does the pain.”

Clinical Snapshot: Acute Lumbar Spasm

• Sudden, well-localised pain (fist-sized), no referral or radicular symptoms

• Often morning onset or after unremarkable activity

• Clear absence of serious red flags (fracture, infection, tumour, vascular)

• Excellent lumbar ROM once spasm resolves, or immediately following simple and gentle manual therapy

• Reassurance and de-escalation trump imaging and intervention

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This blog is written for the clinician who’s halfway through a consult, already sensing that something doesn’t add up. The tests aren’t lining up. The symptoms feel familiar but don’t quite follow the script. And the more you prod, stretch, and ask, the more you realise: this isn’t about finding one magic test — it’s about building a case. We’re diving deep into the art (and science) of separating hip joint, SIJ, and lumbar spine drivers of pain. Not through textbook purity, but through clinical pattern recognition, contextual clues, and a ruthless suspicion of oversimplified labels. If you're here to sharpen your eye for the subtleties — welcome.

You’ve seen the patient: vague pain somewhere around the back, glute, groin, or thigh. The story’s a bit fuzzy. And you’re stuck toggling between lumbar spine, SIJ, and hip joint like you’re playing Guess Who with referral patterns.

This is the Bermuda Triangle of Musculoskeletal Healthcare.

They’ve probably already been labelled—tight hip flexors, twisted pelvis, non-specific back pain. Maybe even all three. Some walk in and thrust the GPs Lumbar Spine CT Scan in your face, and the referral to ‘try some physio’ for their age-related disc bulge (as they start pointing at their hip joint referred symptoms). But you know better: it’s your job to strip the noise, pick up the real pattern, and land the right diagnosis.

This blog isn’t a full deep dive into every possible cause of lumbopelvic pain. It’s a clinical walk-through to help you sort the big three suspects—the hip, the SIJ, and the lumbar spine—when they all start sounding the same.

At the very least, this blog will be helpful at making some connections in your mind and help you find the pattern you were looking for.

Pain in the lower back, buttock, and hip region often leads to diagnostic confusion, given the overlapping referral patterns of the Hip Joint, sacroiliac joint (SIJ), and Lumbar Spine. But if you've been in clinic for any length of time, you'll know there's usually a way to tease them apart—if you ask the right questions, listen properly, and test smart.

There’s so much overlap that site of pain alone doesn’t help—not without context.
Here’s a hot tip: Never trust what the patient is saying.
“WOAH NELLY! HOW DARE YOU!” I hear you say. Give me a second, and I’ll explain:

Don’t trust what they say—trust where they show you. Watch their hand. Ask them to point.
And listen to how vague they are. The patient is often apologetic about that vagueness, but I thank them for it: vagueness speaks volumes. Some pain sources are loud and specific. Others mumble.

If the story sounds fuzzy, it’s often because the joint talking to you has a broken microphone.

Despite being underseen - SIJs (Sacroiliac Joints) are often over diagnosed (especially by those obsessed with pelvic manipulation techniques). The Hip Joint? Often the most poorly recognised major joint—especially in younger non-OA cases. It’s the ‘middle child’ of MSK—ignored, misunderstood, and always trying to prove itself.

Quick Ratio Check (based on clinic experience in private Msk practice):

• 1 SIJ for every 18 hips for every 20 Lumbar Spines.

The key thing is, most of this is a matter of ruling out* as much as possible then trying to make the best of what’s left on your Guess Who board.

Specifically, during the physical examination: the Hip Joint is the easiest to rule out*, followed by the Lumbar Spine (for mechanical low back pain, not so much Spondyloarthropathies), and the SIJ is extremely difficult to rule out.

*OK, let’s pause for a reality check.
Throughout this blog I’m going to sound super dooper confident and say things like:
“Rule out” or “Rule in.”
Every time you see that, I want you to hit Ctrl+H in your brain.
Replace “Rule out” with: Consider much less likely.
Replace “Rule in” with: Consider much more likely.
That’s how clinical reasoning actually works—we’re dealing in probabilities, not absolutes.

A Quick Word on Diagnostic Imaging

Those who rely on imaging alone for diagnosis are doomed to misdiagnose. Imaging should always be interpreted in the context of clinical assessment. "Degeneration"—radiology-speak for age-related changes—is everywhere, especially in people who, well... have aged.

There’s a Butt-tonne of Ass-ymptomatic people walking around with backsides that don’t look great on imaging. Here's the kicker: most of them feel fine.

In the lumbar spine: A systematic review by Brinjikji et al. (2015) found that signs like disc degeneration, disc bulges, and facet joint changes were seen in high percentages of asymptomatic people. For example, disc degeneration was found in 37% of 20-year-olds and up to 96% of those in their 80s. (Brinjikji et al., 2015)

In the SIJ: CT imaging showed sacroiliac joint degeneration in 65.1% of asymptomatic adults, with substantial degeneration in 30.5%—and 91% of those in their 80s. (Eno, Boone, Bellino, & Bishop, 2015)

In the hip: Studies show cam deformities in 37% and pincer deformities in 67% of asymptomatic individuals. That’s before you even touch on the incidental labral tears and signs of impingement in people with no symptoms. (Frank et al., 2015)

Imaging might show you a mess—but it doesn’t tell you what hurts. That’s your job.

So before you treat the scan, treat the person. Use your ears, hands, and brain. Because diagnosing from an image is like treating a shadow—you’ll always miss the mark.

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