You can print and fold the guide into a booklet, or just give your patients the link/QR code to your name-stamped site.

Best wishes,

Tom

‘Degenerative changes’ doesn’t just mean wearing away, it also means growth. Knobbly osteoarthritic knees are a good visible example of this apparent paradox.

The same thing happens in the cervical spine.

Just as skin dehydrates and sags with age, intervertebral discs dehydrate and flatten (1–3). As a disc flattens, the vertebrae above and below it press into each other more. “Settling like a pile of dishes”, as the great physiotherapist Gregory Grieve put it (4). The bony surfaces now bear more and more load.

In response, those bony surfaces thicken, much like skin forms calluses when overused. This new bone has a “brittle, sugary consistency”, as one early description from the 1950s puts it (5). It forms on facet joints, on uncovertebral joints, and extends into spurs on the posterior lips of vertebrae.

These bony extensions are useful in one sense: they support the spine against thinning discs. But they also crowd out the spinal cord. “At operation, when the dura is opened, the cord is found kinked and displaced backwards” (5).

Meanwhile, as discs flatten, the whole cervical spine shortens, and the already thickened ligamentum flavum slackens and buckles into the canal (2). Narrowing discs also bulge outwards.

So three kinds of structures end up encroaching on the cord:

• bone, in the form of spurs and thickened joint surfaces

• ligament, slack and buckling

• disc, narrowed and bulging

The spine’s attempts to adapt to disc narrowing have become the cause of the problem. Yesterday’s solutions become today’s problems.

Mechanical stress on the cord

Bone, ligament and disc encroachment are usually described as compressing the cord. True, but these changes also add tension, shear, and even torsion (6). A bone spur pressing into the cord might cause myelopathy not where the cord is compressed, but on the opposite side where the cord stretches (7).

Neck movement adds dynamic stress on top of the static. When you flex your neck, the cord stretches over those degenerative changes. When you extend your neck, it gets pinched by them. Bone spurs create “deep grooves” in the cord’s anterior surface, says Alf Breig, forming “humps” on the posterior side (7).

This variety of stresses helps to explain why DCM varies so much:

• between individuals

• week to week in the same person, in the early stages

• between limbs in the same person

It is also part of why no single test reliably detects it (8).

What happens to the cord?

All this mechanical stress squeezes blood vessels and chokes the cord’s blood supply (2,8). The first surgeons to document DCM described how the cord blanched under stress points (5,9). “On flexing the neck there was posterior displacement of the cord, producing pallor” (5), wrote one.

Starved of blood, neurons lack oxygen and can’t fire. It’s similar to sitting with your legs crossed for too long, reducing blood flow to your peroneal nerve and giving yourself a temporary numb, floppy foot.

With DCM, blood vessel walls grow thicker to adapt to the chronic mechanical stress. But in doing so, the space inside the vessel shrinks. So even as blood vessels try to adapt, the cord is starved for oxygen.

Eventually, lacking oxygen and surrounded by inflammation from a damaged blood-spinal cord barrier — through which fluid and inflammatory cells leak into the cord tissue itself — neurons and their support cells die (6,8).

A paradox: weakness and overactivity

Upper motor neurons do two jobs at once. They drive movement, and they control it: tapping the brakes to inhibit muscle contractions, dampen reflexes, and relax tone. When UMNs stop working, you lose both the drive and the brakes. So in DCM, the legs are weak and in a constant state of agitation.

This is why we see jumpy reflexes. From just a light tap, the knees jerk dramatically. The calf muscles may contract rhythmically — clonus — because the reflex is so sensitive that it elicits itself over and over in a cycle. When the sole of the foot is scratched, the big toe curls upwards: Babinski’s sign, normally seen only in neonates, re-emerges when corticospinal inhibition is lost (12).

Combine the hypertonia, hyperreflexia and the weakness, and you get myelopathic gait (13–15). It’s often:

• short-stepping: weakness shortens stride

• stiff: hypertonia

• slow: weakness, again

• shuffling: less toe clearance, what one author calls a “spastic foot drop” (13). Falls are often the first reason the myelopathic patient presents to the health system

• strenuous: every step is work

Numbness in the legs makes everything worse.

Patients say:

“My legs are like jelly.”
“It’s like I’ve had too many pints!”
“I keep wandering to one side.”
“I’m dragging my legs.”
“I’ve had to start using a stick...”

The same paradox in the arms

When upper motor neurons in the neck become damaged, the arms develop the same pattern: simultaneous rigidity and jumpy reflexes from lost inhibition, weakness from lost drive.

A light flick on one digit elicits a reflex in another: Hoffmann’s and Tromner’s signs. Movement becomes stiff, slow and strenuous. Doing up buttons is a classic difficulty.

In clinic, ask your patient to:

• rapidly open and close a fist

• hold and extend the fingers

• tap a finger (9,16,18)

Patients say:

“My arms feel dull.”
“I can’t feel my fingertips.”
“I can’t use a knife and fork like I used to, I’m getting so clumsy.”
“My hands shake.”

To compensate for lost dexterity, larger joints — wrist, elbow and shoulder — take over movements that should require only fine motor control (19).

The arms differ from the legs in one important way, though. For the legs, the cervical cord is just a highway: upper motor neurons passing through. For the arms, the cord is also a nerve root entry/exit point.

Lower motor neuron cell bodies sit in the ventral horn and their axons exit through the ventral roots, while sensory axons enter through the dorsal roots from their cell bodies in the dorsal root ganglia just outside the cord. So cervical degeneration in the arms can also cause nerve root problems: radiculopathy.

Radiculopathy is different to myelopathy because there’s no hyperactivity. It’s a more straightforward loss of function: weakness, decreased reflexes.

Which means, paradoxically, that at the actual level of degeneration, a patient with DCM might have none of the expected hyperreflexia or hypertonia. There’s a radiculopathy, with its pure loss of function, at the myelopathy point.

Nerve root symptoms

With nerve root injury comes nerve root symptoms. A few are worth keeping in mind:

• Transient tingling in the hands, often with numbness. Frequently misdiagnosed as carpal tunnel syndrome (3).

• Scapular pain (20): pain referred from the spine to the shoulder blade, commonly misattributed to local muscle problems like trigger points or rhomboid strains. Similar to how spine-referred buttock pain gets mislabelled as gluteal or piriformis issues.

• Radicular pain: distal, severe, neuropathic. The worst of the nerve root symptoms. But unlike disc herniations, where inflammation drives immediate pain, DCM doesn’t always produce radicular symptoms. Tingling is more common.

And what about neck pain? It’s common, as it is for all older adults. But it’s often not as serious as you might expect. “It is rare for pain, stiffness, or limitation of movement of the neck to be an outstanding symptom”, one doctor wrote in 1955 (21). “Examination of the neck commonly reveals little abnormality.”

A normal neck assessment does not exclude DCM.

The atypical

Even this is only the shallow end. Patients also report:

• sensory disturbances — “a wet gel substance”, says one (22)

• sciatica (23)

• altered temperature sensation

• nausea and vomiting

• difficulty breathing

• cranial nerve symptoms: difficulty swallowing, dizziness, headache, tinnitus, face pain and numbness (20)

These symptoms might be downstream effects in the brain, or autonomic dysfunction. Or they might arise because the blood vessels supplying the cord criss-cross spinal levels, so a single local stress point can starve a much wider region of oxygen (8).

“There is less correlation than might be expected between the distribution of the [myelopathic signs] and the site of the lesion”, wrote Walter Russell Brain in 1952, in one of the first papers to describe DCM (24).

At least we have a decent understanding of the basics.

***

Thanks to John Drummond for his help with this post. A different version appeared in MSK Mag.

References

1. Nouri A, Tetreault L, Singh A, Karadimas SK, Fehlings MG. Degenerative Cervical Myelopathy: Epidemiology, Genetics, and Pathogenesis. Spine. 2015 Jun;40(12):E675–93.

2. Tetreault L, Goldstein CL, Arnold P, Harrop J, Hilibrand A, Nouri A, et al. Degenerative Cervical Myelopathy: A Spectrum of Related Disorders Affecting the Aging Spine. Neurosurgery. 2015 Oct;77(Supplement 1):S51–67.

3. Clarke E, Robinson PK. Cervical myelopathy: a complication of cervical spondylosis. Brain. 1956;79(3):483–510.

4. Grieve GP. Common vertebral joint problems. Edinburgh: Churchill Livingstone; 1981.

5. Allen KL. Neuropathies caused by bony spurs in the cervical spine with special reference to surgical treatment. J Neurol Neurosurg Psychiatry. 1952 Feb;15(1):20–36.

6. Davies BM, Mowforth OD, Smith EK, Kotter MR. Degenerative cervical myelopathy. BMJ. 2018 Feb 22;k186.

7. Breig A, Turnbull I, Hassler O. Effects of mechanical stresses on the spinal cord in cervical spondylosis: a study on fresh cadaver material. J Neurosurg. 1966 Jul;25(1):45–56.

8. Badhiwala JH, Ahuja CS, Akbar MA, Witiw CD, Nassiri F, Furlan JC, et al. Degenerative cervical myelopathy — update and future directions. Nat Rev Neurol. 2020 Feb;16(2):108–24.

9. Crandall PH, Batzdorf U. Cervical spondylotic myelopathy. J Neurosurg. 1966 Jul;25(1):57–66.

10. Karadimas SK, Gatzounis G, Fehlings MG. Pathobiology of cervical spondylotic myelopathy. Eur Spine J. 2015 Apr;24(S2):132–8.

11. Lees F, Turner JWA. Natural history and prognosis of cervical spondylosis. Br Med J. 1963 Dec 28;2(5373):1607–10.

12. van Gijn J. The Babinski sign: the first hundred years. J Neurol. 1996;243(10):675–83.

13. Rubino FA. Gait disorders. The Neurologist. 2002 Jul;8(4):254–62.

14. Maezawa Y, Uchida K, Baba H. Gait analysis of spastic walking in patients with cervical compressive myelopathy. J Orthop Sci. 2001;6(5):378–84.

15. Pirker W, Katzenschlager R. Gait disorders in adults and the elderly. Wien Klin Wochenschr. 2017;129(3):81–95.

16. Smith ZA, Barry AJ, Paliwal M, Hopkins BS, Cantrell D, Dhaher Y. Assessing hand dysfunction in cervical spondylotic myelopathy. PLOS ONE. 2019 Oct 28;14(10):e0223009.

17. Good DC, Couch JR, Wacaser L. “Numb, clumsy hands” and high cervical spondylosis. Surg Neurol. 1984 Sep;22(3):285–91.

18. Miwa T, Hosono N, Mukai Y, Makino T, Kandori A, Fuji T. Finger-tapping motion analysis in cervical myelopathy by magnetic-sensor tapping device. J Spinal Disord Tech. 2013 Aug;26(6):E204–208.

19. Durrant DH, Blum JW, True JM. Myelopathy, radiculopathy, and peripheral entrapment syndromes. Boca Raton: CRC Press; 2002.

20. Munro CF, Yurac R, Moritz ZC, Fehlings MG, Rodrigues-Pinto R, Milligan J, et al. Targeting earlier diagnosis: what symptoms come first in Degenerative Cervical Myelopathy? PLOS ONE. 2023 Mar 31;18(3):e0281856.

21. Northfield DWC. Diagnosis and treatment of myelopathy due to cervical spondylosis. Br Med J. 1955 Dec 17;2(4954):1474–7.

22. Mowforth OD, Davies BM, Kotter MR. “I am not delusional!” Sensory dysaesthesia secondary to degenerative cervical myelopathy. BMJ Case Rep. 2019 Apr 1;12(4):e229033.

23. Han C, Wang J, Wang L, Gong Q, Huang W. Sciatica-like pain caused by cervical spondylotic myelopathy: four case reports and systematic review. Front Med. 2024 Aug 1;11:1429618.

24. Brain WR, Northfield D, Wilkinson M. The neurological manifestations of cervical spondylosis. Brain. 1952;75(2):187–225.

Some thoughts:

• Back pain that runs down the leg is common; true sciatica — an irritated nerve in the spine — is relatively rare.

• How do you know if you have true sciatica? It’s usually severe. It’s just as bad, if not worse, below the knee as above it. It often comes with tingling, prickling, numbness, or other unpleasant sensations that aren’t pain.

• The nerve is in your spine, but you feel the pain in your leg because that nerve usually carries signals from the leg.

• Why is the nerve irritated? Some mix of (1) pressure and (2) inflammation.

• Pressure can be anything from a nudge to a squash. In fact, sometimes there’s no pressure.

• Inflammation is the main driver of the pain. Think of a sprained ankle: it goes red, puffy, and sore as your immune system sends blood and healing cells to the area. Something similar happens in the spine and the nerve.

• What would you do with a sprained ankle? Relative rest, then gradually get it moving again. Blood flow helps recovery. Movement signals to the body that you still want to use this ankle, so don’t neglect it. What else? Get sleep if you can; avoid major stressors if you can; eat well and don’t drink too much alcohol. In other words, put your body in a good place to cope. What should you do if you have sciatica? Much the same.

• What causes the irritation? Most often a disc herniation. The watery-solid centre of a spinal disc can sometimes leak out — herniate. When it does, it can touch the nerve (pressure) and irritate it (inflammation).

• The good news: inflammation often helps clear the herniation. That’s part of its job. Or the herniation may just go dormant. (But not everyone gets better; see below).

• Less common causes of sciatica: other spinal injuries that set off enough inflammation to irritate a nerve; arthritis slowly pressing on a nerve; and, rarely, infections or lumps and bumps.

• How long will it last? Many people improve a lot in the first few weeks as inflammation settles. Some have a tougher few months to a year. A few develop chronic pain that never fully goes away or takes years.

• I wish I could tell you which group you’re in. On average, if you can sleep, sit, work, and feel reasonably positive, you’re more likely to do well. Older people don’t necessarily do worse. People with big disc herniations don’t necessarily do worse either.

• Expect setbacks and flare-ups. When they come, don’t assume you’re back to square one.

• Clinicians diagnose sciatica in the clinic. Most of the time, you don’t need an MRI. If your doctor/PT/chiro didn’t order one, you’re not necessarily being fobbed off.

• MRIs can confuse as much as clarify. Most adults, even healthy young adults, have incidental findings. Many clinicians prefer to stick to the clinical picture: you, your symptoms, the exam, and the trusty reflex hammer.

• Sometimes though, an MRI is essential. For example, if there are ‘red flags’ — specific changes in, for example, bladder or bowel function — or if you’re considering surgery or an injection.

• A common but unfounded regret: “If only I hadn’t [played so much football/lifted weights/run so much], I wouldn’t have had that disc herniation.” Extremes of activity can raise risk, yes. But disc herniations also reflect (1) genetic predisposition, (2) systemic health (illnesses, smoking, diet), and (3) past spinal trauma—falls or accidents, even long ago.

• Moderate exercise and movement are good for discs, as with muscles and joints. When does helpful movement become harmful? We don’t know. For any one person it depends on genetics, general health, and past spinal trauma.

• Disc herniations are most common in the middle decades of life. Having one in your thirties doesn’t mean you’ll keep getting more as you age. Getting older will still have its downsides, but not because your discs inevitably keep herniating.

Part 2 of [?] to come.

As a reminder, I’m working on a free Sciatica Atlas for clinicians, a booklet for patients, and giving an ‘essentials’ lecture in December - come!

Til next time,

Tom

An earlier version of this post originally appeared in MSK Mag.

It all starts in the 1930s, in Massachusetts [1] [2]. A surgeon sees a patient who has developed acute sciatica after a skiing accident. The surgeon, William Mixter, operates on the skier's spine and removes a piece of whitish gunk. Mixter had removed this kind of material before, and he knows what it is: a benign tumour.

But then the skier's doctor gets involved. The doctor, Joseph Barr, says that Mixter’s benign tumour diagnosis doesn’t sound quite right. A tumour should cause insidious pain, but the skier's pain had started suddenly, after an accident.

They look more closely at the whitish gunk from the skier’s spine, and at a lot of other pieces of similar material that Mixter had kept from previous similar operations. And they realise that all these pieces of gunk are, as Barr guessed, not tumours at all. In fact, they're disc material. Disc material that has burst out from its home in the centre of the intervertebral disc.

Too Much Load

Mixter and Barr’s discovery sets the template for our early understanding of what causes disc herniations: that they’re the result of a trauma. In 1938, for example, one physician writes that "It is the opinion of most authors that abnormal protrusion of an intervertebral disk into the spinal canal is in the majority of cases the result of trauma" [3]1. By trauma, most physicians mean something sudden, but some also mean gradual trauma by repeated insults over time; the "slight shocks of normal life"[5].

Whether sudden or gradual, the earliest understanding of why discs herniate is essentially this: too much force goes through the disc, which makes it break. Let's call this school of thought the ‘Too Much Load Camp’.

It only takes a few years for many in the Too Much Load Camp to appreciate that only a minority of people with disc herniations actually report a trauma [6] [7]. As early as 1948, Falconer writes that trauma has been “overemphasised” [5]. Another physician notes that "70-80% of patients give no history of injury. It is reasonable to assume that injury is never the sole causative agent and, when evident, is only an additional factor" [8].

Unhealthy Disc

Where do mid-century physicians go when they leave the Too Much Load Camp? Well, they had long observed that while some discs stay plump, white and healthy, very early in life some others become thinned, yellow and fissured. And they see that these particularly unhealthy discs have slipped into a nasty state of imbalance between catabolic and anabolic activity. They label them as degenerated [8][9].

If it’s not trauma that makes discs herniate, they hypothesise, then it must be this degeneration. “There are other more important basic factors [than trauma]”, writes Naylor in 1962, “herniations most probably develop as a result of a more general collagen/polysaccharide disorder”. In other words, it’s not the load placed on the disc, but the qualities of the disc itself that cause it to weaken and fail. Let’s call this new school of thought the ‘Unhealthy Disc Camp’.

So if the Unhealthy Disc Camp says that degeneration causes herniations, then what causes degeneration?

It’s partly, they say, systemic health. If you smoke, drink, have diabetes or vascular diseases, sleep poorly, work more than you rest and so on, then your discs have an even harder time maintaining themselves [10–13]. Smoking, for example, reduces the metabolic activity in your discs and weakens their structure [14–16].

And it’s partly just that discs are particularly vulnerable to degenerating because they are avascular [11]2.

All In The Genes

Let’s fast forward to the nineties. Researchers have long suspected that disc degeneration is hereditary [8], and a group in Finland decides to find out. They recruit lots of sets of twins with different exposures to the usual risk factors for disc herniations [17]. For example, maybe one twin is a farmer and the other is a reporter; or one is a smoker and the other isn't. Then they put all the sets of twins in MRI machines to look at their discs. And they see that lifestyle factors have barely influenced those twins' discs at all.

With the Twin Spine Studies, what we can call ‘All In The Genes Camp’ is formed. “61% of the variance in disc degeneration is explained by familial aggregation”, the authors write a few years later, summarising their findings. “Disc degeneration, which was once viewed as a result of ageing and ‘wear and tear’ from mechanical insults and injuries is now viewed as being determined in great part by genetic influences" [17].

How does your genetic makeup make you more likely to have a disc herniation? People in the All In The Genes camp don’t claim that there's one gene for disc herniations, but that you might be predisposed by a complex interplay of multiple genes [18] [19]. Those multiple genes might, for example, conspire to make your discs’ collagen matrix weaker, or make the enzymes in your discs more active. That means that ultimately, as you get older, your discs are going to do what they’re going to do - whatever your occupation or smoking status.

But it’s easy - and common - to overstate genetic influence on disc herniations.

For one thing, the estimate of familial influence on disc degeneration in the lower lumbar discs, i.e. the ones that herniate the most often, was just 32% [17]. That’s hardly a slam dunk for the All In The Genes.3

To be clear, the Twin Spine Studies’ estimate of occupation and lifestyle factors is much, much smaller than its estimate of familial influence. So genetics is clearly extremely important. But the studies’ biggest category of influence on lower lumbar disc health wasn’t, in fact, familial influence. It was just labelled… ‘Unexplained’!

Could there be something here for the Too Much Load camp?

Too Much Load Revisited

True, the evidence suggests that occupational and recreational loading has only a modest (but non-zero) effect on disc herniations [25–28]. But research into occupational and recreational exposure can’t account for brief, one-off spikes of excess load: a weekend spent moving house, for example, or a slip on the ice… And some researchers argue that it’s just these spikes of excess load - injuries, essentially - that are pivotal in the life course of a disc, and can set it on the long path of structural failure and eventual herniation [29–31].

And Too Much Load theory does explain something that genetics cannot: why so many people have just one or two herniated discs, while the rest of their spine is fine; and why those herniated discs are frequently the lower lumbar ones, i.e. the ones that work the hardest [32–34]. As Adams and Dolan argue, the most parsimonious explanation for this is discrete trauma [30].

This all flies in the face of the prevailing optimism, in some quarters, that discs adapt well to load and heal from injuries. And it’s true of course that discs adapt; it would be strange if they didn’t [35]. But they don’t do it that well. The best evidence that discs get healthier with exercise is all in recreational runners [36–38], but recreational running is the exact type of predictable, moderate load that lab studies tell us their discs should love [39], and therefore adaptation to running is hardly good evidence of discs’ anabolic power more generally4.

And when it comes to healing from injury, well, they definitely can’t do that. “Adult discs are incapable of repairing gross defects”, write Adams and Roughley [30]5.

Tyre-d of fighting

Joseph Barr, the doctor we met earlier, the one who started all this trouble back in the 1930s, never threw his lot in with any of the three camps. In 1951 he explained his position by likening disc herniations to a car tyre failure:

“The tyre, when it leaves the factory, may have a defect in the fabric (congenital weakness) so that it blows out while rolling along a smooth road. A tyre may blow out when it strikes a stone or curb (acute trauma), or it may give way thousands of miles later. A tyre exposed to gasoline ages rapidly, and degenerative change produces early tyre failure [42]".

Genetics, or ‘congenital weakness’ as he calls it, turned out to be far more important than Barr expected; but his analogy still holds. It captures well that while the various causes of disc herniations are interrelated, each one might predominate in different cases. Back to the patient’s story.

Reference list: click here

More detail on lifting, bending & disc herniations: click here.

Thanks to Felicity Thow for help with editing this piece.

Like many sciatica stories, I had a history of rumbling, on-off back pain for a few years before anything started in my leg. The first time I ever got proper back pain, it was because I fell out of a tree. I was too old to be falling out of trees: twenty-one. I fell right on my back and couldn’t move for about ten minutes. In the next few years I’d have about one episode a year, usually triggered by exercise.

The sciatica started when I was about twent-six. I was deadlifting. I remember being tired that day, but I tried to do one more rep than I was planning to. I felt something go. I immediately packed everything up, got changed and went home as quickly as I could before everything seized up.

The back pain calmed down after a couple of weeks. As it calmed down, the leg pain started.

That’s a pretty common pattern for extrusions. The theory is that the back pain is caused by the disc material pushing through the inflamed rupture in the outer layers of the disc. Once it finally pushes through and out, the disc can start to calm down and heal, so the back pain dies down. But now the material is on the root, so the leg pain starts up.

The leg pain was never that bad. It was an aching or tugging down the back of my leg into my calf. I guess you’d call it neural sensitivity or mechanosensitivity; the nerves of the nerve were sensitive. But no neuropathic pain. The injured nerve root never developed a hot-spot to send crash-cymbals of action potentials up to my brain.

It was a while before I worked out I should sleep and sit with my legs curled up. I was a physio student at this point. We hadn’t studied this yet.

I never felt that worried. I’ve been ill and injured before when I’ve felt a sense of dread and doom, not to mention severe pain. I also catastrophise about stuff at times. But I was never that worried about this. I was more just annoyed about it.

I went to see a physio. I’m not sure I would have done except I saw it as an opportunity to learn as a patient from a local physio with an excellent reputation. I was surprised when he demonstrated that my plantarflexion was markedly weaker on my affected left leg. He sent me for an MRI because there was enough other stuff going on that I might have had inflammatory spondyloarthropathy. The MRI showed I didn’t. I had a big disc extrusion.

I think the MRI might have been the most unpleasant thing about the whole affair. You can never unsee your MRI scan. I think the fact that the remaining disc was just black, so different to the others, bothered me more than the extrusion. This load-bearing aspect of my anatomy was now a failed joint?

The physio advised I keep going to the gym, which I had been doing. But to avoid stretching out my nerve while loading my back, I should stop squatting for a few weeks and deadlift off pins. That did take the edge of the post-workout flare-ups.

He also recommended neurodynamics, which I did regularly throughout the day. I’m not sure they helped but they didn’t do any harm. Maybe they kept the nerve mobile and prevented adhesions.

He didn’t recommend any core stability exercises. But I did keep doing core exercises, as in ab and back exercises - just not the rehab ones, like the McGill Big 3.

(By the way, I kept in touch with that physio and he ended up as my co-author, we wrote a book on CES together).

I also did a lot of Jefferson curls. I imagined curling my spine down and vertebra-by-vertebra. With just a 10kg bar. I think they had a good psychological effect because they reassured me that the supposed worst movement could actually feel kind of nice. They also helped me ‘practice movement’ again, working through little catches of pain or parts I was holding stiff. They probably had some physiological effect too by preventing or reversing some spinal muscle weakness. (All this could also be said for the core exercises I kept doing, too.)

Getting back to running was a case of building up slowly, doing too much, cursing myself, resting for a few days, then building back up even more slowly.

I can’t even remember the rest of the story. The pain just gradually died down over the next couple of months. I think there were one or two little blips where it threatened to come back.

That was now almost a decade ago.

Today, my left-sided plantarflexion is still slightly weaker, and, although it’s my jumping leg, that leg is still not as springy when I skip (jump rope). If I work in the garden too long my left calf starts to throb again.

I still have a little thing in my head that tells me to worry about my back in a way that I don’t worry about any of my other joints. It’s always there. But it’s extremely low-level. What’s less than a worry? A subdued awareness. Almost subconscious.

I think the radiculopathy was the end of my back pain story. If I could place a bet, I think all my back pain episodes were sparked by the fall, which set off (or accelerated) some disc degeneration. The yearly episodes in my early twenties were probably the gradual progress of degeneration and herniation. The culmination was the eventual extrusion, which caused radiculopathy.

Since that resolved, I’ve had almost no spinal pain. I feel like that disc’s dance is done. It hasn’t rehydrated (it can’t), but the inflammation has died down and there’s not enough internal pressure to force out whatever nucleus is left, if there’s any.

I still squat and deadlift. (Very modest weights, but they always were - you are definitely not reading the story of an athlete here). I run and play sports and pick up my children and throw them in the air - all with that ‘subdued awareness’ of my back. If I’m lifting anything above, say, 60 pounds, I consciously brace my back and posterior chain in a way that some physios might consider an undesirable ‘safety behaviour’, but it works for me. My back feels better when I do.

I do see how lucky I am that 1) I never got proper neuropathic pain, and 2) this just resolved by itself. I can take some credit for not doing anything too stupid while my body recovered. And for being pretty healthy when it started. But the rest is good fortune.

Most people who get radiculopathy are lucky, though. I didn’t do anything special and I got better anyway, just like people and proto-people have been doing not much very special and getting better anyway since our mammaliaform ancestors first developed intervertebral discs, however many hundreds of millions years ago.

One of the first recorded cases of sciatica might be in Genesis. Jacob fights an angel and the angel touches the hollow of his thigh, on a 'sinew' that is probably the sciatic nerve. Jacob's leg buckles and goes limp. We never hear whether Jacob gets better. But given that he goes on to travel the known world extensively on foot, we can assume he recovered. It is unlikely he did any core stability exercises.

Mine is a very ordinary story, as old as time.

A year of good work:

• Lower limb neuro exam interview

• Zine on the neuro exam

• Zine on the straight leg raise

• Long post: does bending and lifting cause disc herniations?

My reflections: I always want to do more, but I never can seem to. The harvest is plentiful, but the labourers are few. That said, I’m pleased that my work continues to be of the highest quality.

Next year:

• Cervical myelopathy zine

• Patient-facing info

• Translations of existing work

Happy new year!

Tom

[UPDATE: a new review on this topic supports the conclusions in this post].

Does lifting and bending1 cause disc herniations?

Two groups argue over the science.

One group say that lifting and bending do cause herniations, so we should avoid them (to a lesser or greater extent). Keep your spine in ‘neutral’, and don’t overdo it. Let’s call this group the Cautious Kennys.

The other group say that lifting and bending do not cause herniations, so we shouldn’t avoid them at all. Lift, bend, heave and stoop away! Let’s call this group the Cavalier Karens2.

Let’s watch them argue it out.

Battle 1: Dead discs vs computer discs

The Cautious Kennys didn’t make up their message of caution out of nowhere just to scare everyone. Decades of research shows that bending and lifting are one route, probably the main route, to a disc herniation3. If you take dead pigs’ discs, or dead sheeps’ discs, and put them in a disc-flexing machine, and then flex them over and over again - simulating cycle after cycle of bending and lifting - they do indeed herniate in just the same pattern that we see humans’ discs herniate.

Why does that happen? Well, the inside of a disc, the nucleus, is a kind of watery, semi-fluid substance. It has the consistency of phlegm, or porridge, or toothpaste, or watery crab’s meat, depending on who you ask. When you’re standing up straight, the watery nucleus accepts all the force of bodyweight, muscle contraction, and anything you’re carrying, and pushes that force outwards in all directions.

But when you bend forward, the watery nucleus pushes almost all of that force in one direction: backwards. And when you bend forward and lift something heavy, that adds even more force to the equation. So bending and lifting is double trouble. If you do it enough, say the Cautious Kennys, then all that backward-directed force will start to tell… the watery nucleus will prod and push through the more solid outer part of the disc, eventually escaping through the outermost layer - splurge! - and into your spinal canal. Which is a disc herniation.

Cautious Kennys take this to mean that bending and lifting are the main route to disc herniation, and that we should therefore avoid them.

How could Cavalier Karens argue with that? Well, they point out that there’s only so much you can reason from dead discs in lab conditions. When you use computer simulations to add in the push and pull of the muscles, ligaments etc. that surround the disc, the Cautious Kennys’ picture is not so simple. Sure, if you avoid bending to lift then you might, theoretically, reduce the amount of force your nucleus pushes backwards… but in doing so you only increase the amount of force going through the spine in other ways.

For example, let’s say you have 50 boxes to move into a U-haul. You don’t want to bend your low back, so you lift with a nicely extended low back. According to Cautious Kennys’ theory, this reduces the amount of backwards-pressure that pushes through you discs. But, in order to keep your low back in that nice extended position, you have to contract your spinal muscles a lot more. In doing so, you scrunch more force through the disc, i.e. the force of that extra muscle contraction. And that’s not all: with all the extra effort it takes to keep your low back in a nice extended position your muscles will fatigue earlier, leaving you vulnerable to an overuse injury!

In other words, there’s no get-out-of-injury-free card! Reducing risk in one way only adds it in another.

In fact, some radical Cavalier Karens argue that you should deliberately lift with a rounded low back, because that allows the ligaments of the spine to take up some of the load of those boxes, just as they were designed to do! This makes lifting with a rounded low back more energy efficient. Cautious Kennys are ready for this one though: they would reply that deliberately lifting with a bent low back is a bad idea because, once you’re got about 25 boxes in that U-haul, your ligaments will start to stretch and slacken. Now they’re not doing their job as well, and you’re inviting an injury that way!4

So this battle has turned into a bit of a melee. There’s no get-out-of-injury-free card; lifting technique - whether it’s a bent or extended spine, or a squat or stoop approach - is trade-offs all the way down.

Now, do I believe that that all lifting postures are the same, that it’s all just relative? Not really, I’m sure if we had a computer with the Eye of God that could model this all a billion times then it would tell us that some positions are worse than others, and this might very well be bent-spine lifting5. But what seems clear, once the Cavalier Karens have presented their evidence, is that there’s no categorically safe position and no categorically dangerous position, because making yourself (theoretically) safer in one way only increases (theroetical) danger in another way.

And that’s not even accounting for the fact that, no matter what lifting style you adopt, bending your low back is inevitable! Yes, perhaps suprisingly, even when you do a perfect ‘manual handling approved’ lift the low back is probably flexing. [H/T Greg Lehman]. So to a certain extent the debate about whether to try to avoid low back flexion is moot when some flexion is inevitable anyway.

So what should you do? Well, from a biomechanical point of view, a sort of ‘freestyle’ attitude to lifting and bending is probably best. That means being comfortable, both physically and mentally, in a very bent or very extended position, but that spends most of the time in the large range between the two6. A kind of ‘master of all positions’. You can think of this as having a range of different movement strategies to get the job done and to switch between to distribute the load.

So who wins Battle 1; is flexing and bending really worse for the disc? Well, I do think that Cautious Kennys are correct: all else being equal, bending while lifting is probably is ‘the disc herniation position’. It’s hard to argue with the ‘pop’ of a sheep’s disc as it herniates after its 10,000th flexion cycle. But, with their computer models, Cavalier Karens have demonstrated that lifting and lifting posture are far more about trade-offs in different directions than ‘avoid The One Bad Thing and do The One Good Thing’. This seriously calls into question whether, out in the real world, avoiding bending and lifting is a reasonable strategy to avoid disc herniations.

Verdict: a mellee ending in a draw

Battle 2: Eager little adapters?

Sensing weakness, the Cavalier Karens move to seize the advantage. ‘This biomechanics talk is all moot anyway’, they say, ‘we aren’t dead pigs’ spines, we are living, moving, breathing human beings.’ (Some Cavalier Karens have a sentimental streak to them). ‘And people adapt to load. With bending and lifting, our discs get stronger - just like muscles and bones!’

To prove this point, Cavalier Karens usually point to a number of studies that show that runners, and perhaps some other athletes, have slightly healthier discs. And conversley, people who don’t exercise have unhealthy, more degenerated discs. “The disc lives by movement, and dies by lack of it”, to quote an old authority7. An extreme example: astronauts’ discs, which, without gravity, feel almost no force at all and therefore swell up unnaturally, which makes them particularly prone to herniation on returning to earth.

But the idea that discs are eager little adapters is not true.

For one thing, just because people who run more have healthier discs, doesn’t mean the running made their discs healthier. It’s more likely that runners are just generally-healthy and genetically-lucky people who also have nice looking discs. And anyway, a trial that tried to make peoples’ discs healthier by running didn’t find any benefit.

True, when you study discs cells in a lab, they do like load—but only moderate load at a moderate frequency. Anything more than that, they definitely do not like. In fact, antying more than moderate load is catabolic (i.e. they can’t recover from it and break down on a microscopic level). This is probably why the strongest evidence that exercise is good for discs is in those runners: running is exactly the kind of moderate, controllable exercise that discs would love and benefit from. And in fact, when you look closer at those studies in runners it’s the slow runners and even the walkers with nice looking discs, not the runners doing higher-impact stuff.

So why don’t discs adapt to exercise and movement very well? It’s mostly because there’s no blood vessels in the interior of a disc. The pressure is too high in there. And without blood vessels there’s no ‘supply line’ to get nutrients to the interor of a disc, and no ‘sewage pipe’ to take waste products away. Which means it can’t recover from exercise and adapt as well most other tissues.

It’s even worse once a disc is injured or degenerated (as many tissues are, it’s just part of life). Injured or already-degenerating discs basically can’t adapt to exercise any more. “Adult discs are incapable of repairing gross defects”, write one team of researchers. Another team says that “it is clear that an already damaged or degenerate IVD is unlikely to respond to loading in the same way that a healthy IVD does”.

The Cavalier Karen’s image of discs as eager little adapters who only get stronger with whatever you throw at them is… a mirage. Wishful thinking. The Cautious Kennys are sitting back in their chair looking smug (but with perfect posture).

But I’m being a bit hard on the Cavalier Karens. They are correct to point out that discs like (moderate) movement and exercise, which includes bending and lifting! So the Cautious Kenny idea that we should avoid bending and lifting to ‘protect’ a disc is indeed misguided. Again, there’s no get-out-of-injury-free card! If you avoid bending and lifting to try to protect your discs, you’re running the risk of overprotecting them, denying them the movement they need for their good health.

But, as we’ve seen, the Cautious Kennys are also correct to object that our discs are just not that good at adapting. They can herniate if they do too much too often, and they aren’t that good at recovering from injury8.

So what’s the verdict, are discs eager little adapters? Not at all, but nor are they fragile souls that need to be protected from the world. So this battle is a draw, too!

Battle 3. Out in the real world.

Let’s look at some real-world observational studies. Mostly these studies are of people at work.

Do people who lift and bend a lot have more spinal problems?

Yes. (See here, here, here, here, here, here...)

So, the Cautious Kennys claim a victory? If so, it feels like a hollow one. The association between lifting and bending and spinal problems is modest.

So modest, in fact, that many Cavalier Karens claim the research is a victory for them! ‘Let’s be conservative’, they say: ‘a modest association between lifting and bending and low back pain is tantamount to no association at all. It’s probably mostly issues with the studies: confounding, bias… If the Cautious Kennys were right we would have expected to see a much larger association!’

You might say that the real question isn’t association but causation. Does the research show that lifting and bending at work actually cause spinal problems? Well, here too there’s bitter disagreement on how to interpret the evidence.

For example,

• A review by Bakker in 2009 concluded that association between “heavy physical work, and working with one’s trunk in a bent and/or twisted position and LBP was conflicting”.
  But this review was criticised, mostly for categorising p values of more than 0.05 as evidence against an association, which they are not.

• A review by Wai et al. (2010) said “the evidence suggests that occupational bending or twisting [or lifting] in general is unlikely to be independently causative of low back pain”.
  But this review was also criticised for 1) using a extremely high bar to prove causation, effectively setting the hypothesis up to fail given the state of the evidence reviewed, and 2) confusing the statement “there’s not enough evidence for us to say whether bending and lifting causes LBP” for “bending and lifting does not cause LBP”.

• A scoping review by de Bruin et al. (this year, 2024) concluded that “there was insufficient evidence to support a causal relationship between loading and the onset and persistence of [LBP]”.
  But an editorial on the paper gently pointed out that de Bruin et al. had done the same thing as Wai et al. in 2010: setting an impossibly high bar, given the level of evidence available. “Assuming a multifactorial causation of LBP”, the editorial states, “applying the [criteria used by de Bruin et al] to any single factor will always lead to ‘insufficient evidence’”.

That’s all ‘low back pain’. Let’s bring this back to disc herniations and sciatica. Here, things get better for the Cautious Kennys. Because there is a stronger case that bending and lifting does cause disc herniations and sciatica out in the ‘real world’.

• A study by Seidler et al. (2009) found "a positive dose-response relationship between cumulative occupational lumbar load and lumbar disc herniation as well as lumbar disc narrowing among men and women". For men, high exposure to occupational lifting had a 3.4 (2.2, 5,0) odds ratio for disc herniation. In other words, the men in this study who lifted a lot at work were roughly 3.4 times more likely to get a disc herniation. That’s about the same as the odds ratio between smoking and coronary heart disease, or obesity and diabetes, or air pollution and asthma exacerbations.

• A meta analysis by Kuijer et al. (2018) found that there’s "moderate to high-quality evidence is available that [sciatica] can be classified as a work-related disease depending on the level of exposure to bending the trunk or lifting and carrying".

• And a study by Bergman and colleagues confirms by direct comparison that disc herniations do seem to be more associated with lifting and bending than is back pain.

My take: lifting and bending a lot at work does cause low back pain (it would be strange if it didn’t), but a million other things cause/protect against low back pain so whether this is a meaningful cause on a population level is debateable. The case is stronger for lifting and bending causing disc herniations and sciatica, which makes sense because disc herniations and sciatica are much closer to a classic ‘overload injury’ type problem.

That said, remember this is all occupational. I don’t think there’s anything in these studies that says we should avoid day-to-day or recreational bending and lifting, whether that’s picking up socks, children, pickleballs or barbells.

Verdict: the Cautious Kennys take it, although not as emphatically as they’d like.

Battle 4: Cavalier Karens’ Trump Card

The Cautious Kennys fought valiantly, and had more firepower than many of you might have expected… I think they are right that bending and lifting causes disc herniations, but I’d qualify that to extremes of bending and lifting9.

In any case, the Cavalier Karens win a lot of ground in this battle by pointing out this simple fact:

For 99% of people out there, it doesn’t matter who wins a marginal victory on the topic of bending and lifting. That’s because there are other things—three of them!—that are probably bigger causes of disc herniation.

Those three things are:

1. One-time trauma.
   
   A fall down the stairs, a sports injury, or a Sunday spent moving house. These discrete episodes of overload are kind of the ‘dark matter’ of research on this topic. How do you identify and measure them in a scientific way?10 As far as I can tell, most studies don’t.
   
   But from what we know about the mechanics of disc herniations, and discs’ inability to recover from discrete injuries, one-time trauma is a very plausible Big Cause of many disc herniations. It’s not necessarily that a disc herniation would happen all at once just because, say, you fell while skiing. But given that discs are very poor at healing from injury, and staying healthy once injured, it’s likely that such incidents start some discs off down the path to a herniation, or expediate herniations that are already brewing for other reasons.
   

2. General health.
   
   If you smoke, drink, have diabetes or vascular diseases, then your discs have an even harder time staying healthy. Smoking, for example, reduces the metabolic activity of discs and weakens their structure. This might not be obvious but becomes more intuitive when you consider the effect of smoking on skin quality, and then extend that to other tissues in the body including the disc.
   
   In other words, it’s not only the stress placed on the disc (by bending and lifting), but the health and integrity of the disc itself, partly determined by lifestyle, that cause it to fail and herniate11. Strangely, we readily accept this principle for things like major vascular events, osteoporotic fractures and tooth cavities, but there is a cultural blindspot around discs that only allow us to think about load.
   

3. Genetics.
   
   For decades, clinicians have noted that disc herniations seem to run in families. These observations were confirmed in the 90s by the famous Twin Spine Studies. You might have seen the MR images from these studies, of twins who entered very different professions - farmer and journalist, labourer and secretary - and yet ended up with very similar-looking spines. The Twin Spine Studies showed that twins with genes that increase their risk of disc problems—genes that make their discs’ collagen matrix weaker, for example, or make the enzymes inside their discs more active in breaking down the discs’ structure—are more likely to get disc problems no matter how much lifting and bending they do throughout their lives.
   
   (Cavalier Karens sometimes grossly overstate the conclusions of the twin studies, though12. Heredity does play an important role in whether you get a disc herniation, but disc herniations are by no means ‘just genetic’.)

We can call these the Big Four causes of disc herniations: 1) bending and lifting, 2) one-time trauma, 3) general health and 4) genetics13. And bending and lifting is probably the little brother here, although it’s hard to weigh them against each other so I admit that’s a hunch.

Verdict: The Cavalier Karens win this battle. Bending and lifting are a small part of the big picture of disc herniations. And I think given how much territory the Cautious Kennys have lost, the Cavalier Karens are clearly winning this war.

Final message

For most people, this is my message on bending and lifting:

Bending and lifting is one cause of disc herniations.

But it’s a small piece of a big picture. In fact, bending and lifting is probably only a meaningful cause of disc herniations when it’s done excessively, such as with reasonably high-level lifting sports, or with years of occupational exposure.

That means if you avoid day-to-day bending and lifting, you’re probably not getting much benefit in terms of avoiding a disc herniation.

In fact, you might cause yourself problems by 1) relying too heavily on one way of moving, and 2) denying your discs the movement and force they need to be healthy. Do not let your spine wither away to reduce the theoretical risk of a disc herniation that might well happen - or not happen - anyway! “The disc lives by movement, and dies by lack of it”.

What about if you do bend and lift a lot, either at work or for a hobby? Well, other things being equal, you are probably increasing your chances of a herniation. If you are able to make changes to bend and lift less at work, you should do so.

But, even if you are doing a lot of it, bending and lifting is unlikely to be the decisive factor. Whether or not you get a disc herniation is probably more determined by your luck (in terms of whether or not you suffer physical trauma), your general health, and your luck again (in terms of what genes you inherited from your parents)14.

I suppose that makes me a Cavalier Karen.

To Use in Clinic:

The Sciatica Guide (website and/or printable booklet for your patients)

What is Sciatica?

• Basic definitions of radicular pain, radiculopathy & referred pain

• What are we talking about? [link opens pdf]

• *That* nylon thread study

• 🎧 Mechanisms of radicular pain with Annina Schmid

• Why would sciatica take a fortnight to kick in?

• 📘 Understanding Sciatica, book with Annina Schmid ($); in Spanish

General

• 🎧 Conversation with David Butler

• 🎧 Conversation with triathlete and sciatica-haver Kate Charlton (pt 2 here)

• 🎧 Conversation with Mark Laslett

• 📑 Physiotherapy for People With Painful Neuropathies (narrative review with Annina Schmid & Nils Runge)

• Four to Six Schmeeks: How long does sciatica last?

• Five insights from patients

• Piriformis syndrome doubts

• Neuropathic pain

And disc herniations?

• What causes disc herniations?

• Does bending and lifting cause disc herniations?

• What do we actually know about disc herniations and radicular pain?

• A historical perspective [link opens pdf]

Cauda Equina Syndrome

• 📘 CES: The Clinician’s Guide, book with Rob Tyer ($)

• So, uh, what is CES anyway?

• 🎥 Understanding sciatica & CES youtube interview

• What we can learn from three new CES publications

• CES has stages, kind of

• Bladder change in CES: not just incontinence

• 🎥 CES Sessions webinars with Rob Tyer ($)

How to assess sciatica

• How bad are the dermatomes?

• 📔 Differential Diagnosis ‘zine ($)

• 📔 How to do a lower limb neuro exam ‘zine ($) and 🎥 podcast

• 📔 The straight leg raise: much more than you wanted to know ‘zine ($)

Not Sciatica

• Exercising when it hurts (for patients)

• MSCC

• Cervical myelopathy

• Wired into Pain

• Writing advice

• The Curse of Knowledge

Lots more work to be done! Let me know what you want to see in the future, and support the work by buying a book or zine.

Til next time,

Tom

It was a quieter year than usual, but a good one.

Some very popular substack posts:

• What do we actually know about disc hernations and radicular pain?

• Four-to-six schmeeks: How long does sciatica last?

• What can we learn from three new papers about CES?

• CES infographics for new grads

• 10 papers to get started with CES

Other writing:

• A back to basics sciatica terminology post

• What causes disc herniations?, for MSK mag

• Co-authored a chapter in Pain: A Textbook

• Not writing, but a good intro video on youtube

• >1k like twitter threads on differential diagnosis, bladder dysfunction and loss of saddle sensation in CES, dermatomes, piriformis syndrome, and a gruesome medical study

Not writing, but I also ran two mini-course on CES (recordings available) and gave quite a few webinars on the subject.

And of course, Annina and I completed a full re-write, re-illustration and re-publication of Understanding Sciatica.

Looking back at this year, I’m surprised at how much good work I’ve done. I’ve been so busy with other commitments that I had the impression I was producing very little on the sciatica front. But clearly I’ve done okay. And I’m not shy to say that much of what I have done is simply the very best stuff out there on this topic. My main regret is the same as it was last year: I’ve yet to make a start on writing about treatment and management. Let’s see what 2024 brings.

Happy new year!

Tom

Hi everyone,

Last week I recorded a Youtube video with James Armstrong, which I think ended up being a pretty good intro to sciatica and CES. Here’s the link.

I think I’ve picked up a lot of subscribers lately who are new to this stuff. The video above should help, and I also recommend the following links, too:

• Important paper by Bogduk (2009)

• Terminology time

• Downloadable intro zine [free]

• *That* nylon thread study

• E3 Rehab video

• So, uh, what is cauda equina syndrome?

• 10 papers to get started with cauda equina syndrome

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As a brief update on my work - I’m trying to find a way to get going with the third book, which would be on the treatment/management of radicular pain. I’ve been itching to start the book for a long time, and my daughters have recently started preschool which means I finally have a little bit of discretionary time to write it. I think the project will have to be pre-funded this time, likely by presales. I’m hoping to rope in some coauthors, too. As always, the goal is help you as much as possible with your clinical practice. Watch this space!

Til next time,

Tom

Well, the NHS website says:

“Sciatica usually gets better in 4 to 6 weeks”

Spine Health says that sciatica

“May flare intermittently or remain constant for up to 4 to 6 weeks”

According to StatPearls,

“Most cases of sciatica resolve in less than 4 to 6 weeks”

And the British Associaton of Spine Surgeons has this graph, which says that after 4 weeks, nearly 80% of people are no longer complaining of pain1:

Hmmm….!

What does the research say? Well, in this post I’ll lay out some broad conclusions2. And at the end, we’ll come back to the ‘4-6 weeks’ line to see how it holds up!

First conclusion:

There’s a rule of thirds for acute sciatica.

For people with very acute sciatica, there's a rule of thirds: Over the next couple of weeks, you have about a 1 in 3 chance of your pain greatly improving; a 1 in 3 chance of it improving a fair amount; and a 1 in 3 chance of it staying the same or getting worse.

The main source for this conclusion is a study by Vroomen and colleagues, which is one of the few studies that catches people very early after the onset of their pain and follows up in the short term. What did it find? Amongst 183 people with an average of two weeks of lumbar radicular pain, 65-70% said they experienced "any improvement", whether a little or a lot, after two weeks. And 35-37% of them said they were greatly improved. Average improvement was gradual over the two weeks:

We can cross-check the study by Vroomen et al. against an older study by Hakelius, which looked at 447 patients with an acute onset3 of radicular pain and found a very similar pattern of improvement4. It’s worth also mentioning a study by Weber and colleagues, who followed 208 patients with acute radiculopathy and also observed a significant improvement in the first four weeks, in this case measured in mean pain scores:

Both these studies back up the results from the paper by Vroomen et al. and increase my confidence in a rough ‘rule of thirds’.

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Surprisingly, that’s about all the research we have on the very acute phase. What about when we extend the timescale a bit?

There’s a 50% resolution rate within three months.

For about half of all people seeking care with sciatica, pain will resolve, or nearly resolve, within three months.

There are two high-quality, landmark RCTs that find strikingly similar results about when people first feel like their pain has resolved.

The first, the recent SCOPIC trial, enrolled a group with a mixture of acute, subacute and chronic sciatica. (Specifically, the group had had sciatica for an average of two months, with about half the group having pain for more than three months.) After three months of mostly conservative treatment, 50% of the group described themselves as recovered:

The other high-quality RCT is by Peul and colleagues also enrolled people with an average of two months of sciatica, and also found that after 12 weeks, 50% of them described themselves as recovered.

To those two trials, we can also add the previously-mentioned older study by Hakelius, which found that 50% of people were free of symptoms in just two months5

Now, to be clear, this isn’t really natural history any more. Most of these people aren’t being followed from the time of the onset of their sciatica, and they’re also all receiving treatment. Rather than natural history, this is the ‘clinical course’ of sciatica - in other words, ‘what’s probably going to happen from the time of your first appointment on, irrespective of how long your pain has been going on’. It’s not nearly as useful as true natural history, but it’s what we’ve got.6

In any case, it looks like half of all patients with sciatica recover within three months. Or, to put it another way, when you see a new patient with sciatica, there’s a 50/50 chance their pain will be gone or essentially gone in the next three months. And that goes for all patients, whether acute or chronic - but we can assume people with acute pain will have better odds.

The problem, as we’ll see soon, is that once pain has resolved… it might not stay resolved.

But for now let’s stick with the three-four month timeframe… The next consistent finding in the research is:

There’s a 3-4 month improvement window.

The bulk of improvement in pain takes place in the first 3-4 months after seeking treatment.

Pretty consistently7, any patient group with sciatica improves markedly for 3-4 months, then, on average, their pain scores plateau. This goes for both acute groups and mixed acute-chronic groups.

For example, Peul and colleagues found that mean leg pain scores levelled out in earnest at about four months of conservative treatment8.

The ATLAS study found that most improvement in pain took place in the first three to four months, then pretty much immediately levelled off. Patients in this study received a mixture of treatments, including surgery and injections for some.

The SCOPIC trial observed a slowdown in 'first recovery from pain' rate at four months, with a definite plateau 7-8 months in.

There’s more. For example, the seminal Maine Lumbar Spine Study found that there was something of a plateau in improvement after three months, and a clear plateau after one year. Kim and colleagues saw a slowdown in improvement after three months, with a definite plateau at one year. Weinstein and colleagues - same story:

And beyond one year? The plateau keeps on plateauing on9: in their two-year follow-up, Peul and colleagues found there was no more improvement in the number of people saying they were happy with their outcome.

And after five years:

On the other hand, some studies do find slight group-level improvement beyond a year, over very long timeframes. Nykvisit and colleagues found little improvement between one year and five years, but a bit more between 5 years and 13 years. The Maine Lumbar Spine Study finds a slight improvement in outcomes between one year and ten years, but 45% of people in this particularly recalcitrant group (many claiming workers’ comp) still said they had not improved. And an old study by Söderberg found that over a decade there was very gradual group-level improvement:

And there’s no doubt that a minority of people with severe, persistent sciatica do suddenly get better, even after months and years of pain, and sometimes for no apparent reason. This was observed in the ATLAS cohort:

But it still looks like for most people, the bulk of improvement in sciatica takes place in the first three or four months after seeking care. After that, improvement on a group level plateaus, or at least nearly does.

Clinically, what it means is that we can encourage our patients to be optimistic for 3-4 months, but we should help them to be realistic beyond that. Certainly, past the 3-4 month window we shouldn't keep promising people that recovery is 'just around the corner’. Lots of people with sciatica get stuck with their life on hold.

“I think clinicians should be more honest from the beginning when they know there could be a chance of long-term pain. Mine weren’t.” - Patient advocate Tina Price, on her persistent sciatica.

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Let’s continue. Mean group differences are one thing, but patients are probably more interested in their odds of being happy with the outcome. Luckily, we can estimate those…

4 out of 5 people happy after a year.

A year after seeking treatment, roughly 4 out of 5 people are happy with the outcome. Of the 1 in 5 with ongoing symptoms, perhaps half will say things have got worse.

4 out of 5 is a rough approximation of lots of studies.

For example, the SCOPIC study found that after one year, about 75% of people were completely recovered or much better. On the other hand, approximately 18% of patients said they were no better and 7% said they were worse10. Peul and colleagues found that although 95% of patients reported complete or nearly complete recovery at some point in the year of observation, by the end of the year this was only 82.5%, because some of those 95% recovered then relapsed. After five years there was no change.

There’s more: Weber and colleagues found that after one year, 70% of patients with acute lumbar radiculopathy were back at work and unimpeded in their leisure time. Another study by Weber and colleagues found that 80% of people had good or fair outcome. Hakelius and colleagues found that 4/5 of people did not develop long term pain. El Barzhoui and colleagues found a favourable outcome in 84% of patients. In their conservatively-treated group, Weinstein and colleagues found an 82.3% satisfaction rate.

In other words, a fairly consistent 75-85% “I’m pretty happy” rate at one year, which I’ve abstracted out as about 4 out of 5 people.

(Again it’s important to emphasise we are no longer in true natural history territory - many of these patients are receiving routine treatment, and have had pain for some time before the start of the study, so this is really the ‘clinical course’ of sciatica).

(Some studies find a worse than 4-out-of-5-are-happy rate, mostly because they deliberately recruit from a particularly chronic or severe patient group whom you would expect to do worse11. The exception that really bothers me though is the large, high-quality ATLAS study, which reported a measly 55% improvement rate by the end of the year, i.e, far short of 4 out of 5 people. Why? The study population isn’t that unusual, so I don’t think it’s that. Maybe the difference might have something to do with the measure of improvement they used, which was 30% or more on the Roland Morris Disability Questionnaire.)

So, if my estimate of ‘4 out of 5 people are happy with the outcome of care’ is wrong, it’s probably because it’s too optimistic… the true number might be less. Particularly for people with particularly severe or chronic pain.

Let’s continue on a pessimistic note and consider the important fact underlying all these numbers - once sciatica has gone, it doesn’t necessarily stay gone.

20-25% of people relapse.

When sciatica does resolve, there's about a 20-25% chance that it will come back in the next year, although it will not necessarily be as severe.

Suri and colleagues found that amongst 79 people who recovered from radicular pain and remained symptom free for at least a month, 25% had a recurrence in the first year. The pain wasn’t necessarily as bad as their initial attack. Half of these recurrences were in the first three months, and most of the rest were between 4 and 9 months, i.e. recurrences are weighted towards the first year or so. They also found that if people’s pain resolved quickly, it was less likely to recur.

The same team also performed an analysis of another trial, [EDIT - I originally linked to the wrong paper by the same authors here - if you are reading it now, link has been corrected] finding a very similar result: 23% of people who recovered had had a recurrence after one year12. They also found that if someone's pain had resolved completely - no niggling tension or anything - then recurrence risk was lower.

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That’s about the best I could find for pure recurrence rates, but there’s a lot of data out there that confirms that the end of a sciatica story isn’t always, in fact, the end. For example, Peul and colleagues found that fully 23% of patients switched from being happy then unhappy with their outcome, or vice versa.

Söderberg found 40% of his cohort had some sort of recurrence that was bad enough to take time off work, whether a ‘pure’ recurrence or an acute-on-chronic one. Startlingly few people in his study were ‘one-and-done’ - just 14% got sciatica for the first time ever, got better, and never got it again. "Sciatica often runs a remittent course and serious recurrences can occur after years of freedom from symptoms", he writes.

Perhaps the best visual illustration of the twists and turns of a sciatica journey is from the analysis of the ATLAS trial by Ogollah and colleagues. Each green line represents one patient’s leg pain over the course of a year:

I think the lesson here is “this too might pass” - whether you’re recovered or still in pain, whether you’re having a good month or a bad month, there’s a reasonable chance you won’t stay that way.

Summary

In summary,

• For people with very acute sciatica, there's a rule of thirds: Over the next couple of weeks, you have about a 1 in 3 chance of your pain greatly improving; a 1 in 3 chance of it improving a fair amount; and a 1 in 3 chance of it staying the same or getting worse.

• For about half of people with sciatica, pain will resolve, or practically resolve, at some point in the three months after they seek care.

• The bulk of improvement in pain takes place in the first 3-4 months after seeking treatment.

• A year after seeking treatment, *roughly* 4 out of 5 people are happy with the outcome. Of the 1 in 5 with ongoing symptoms, perhaps half will say things have got worse.

• When sciatica does resolve, there's about a 20-25% chance that it will come back in the next year, although it will not necessarily be as severe.

And 4-6 weeks? 4-6 schmeeks!

• Okay, to be fair - the idea that ‘sciatica usually gets better in 4-6 weeks’ isn’t actually that far off, if you pick particular definitions of ‘usually’ and ‘better’! Most people really do feel better in the short term, many of them a lot better.

• But the 4-6 weeks line is probably misleading, more often than not. It hides the fact that 1) about a third of people won’t feel any better in that time frame and 2) the two-thirds that do improve often have a few more weeks/months of niggling pain and recurrances, or worse.

  

• A good alternative to ‘sciatica usually takes 4-6 weeks to get better’ might be ‘The worst pain is usually over in 4-6 weeks, but you’ll probably have some pain for longer. For the majority of people, this is manageable pain that eventually disappears within the year, but for a minority it’s more severe and persistent, or recurring.’ Not as pithy.

• More eloquently, here’s the German surgeon Oppenheim, writing in the 1900s: “In many cases sciatica runs a favourable and rapid course and the patient makes a complete recovery within a few weeks or months. But in other cases the disease is fairly obstinate, it persists for one or several years, and then runs a fluctuating course, and even after healing there is a strong tendency to recurrence.”

The important caveats to everything above are:

• Please think of the numbers in my conclusions as approximations, or rough summaries of trends in the research. They’re not really statistics per se.

• People with sciatica that’s mild or short-lived enough that they never seek care aren’t included in these studies, so they aren’t represented by these conclusions. Similarly, people with sciatica that’s particulary severe, or who have lots of comorbities, are excluded from some of these studies, so they aren’t really represented either.

• Most of these conclusions are drawn from - and therefore can only be apply to - mixed groups of patients with both acute, subacute and chronic pain, i.e. they are about the ‘clinical course’ of sciatica for your average patient seeking care rather than the true ‘natural history’ of sciatica. It’s safe to assume people with acute pain will have better odds and vice versa.

• Probably if you’re going to tell your patients these numbers you should be clear they apply to population averages, and then perhaps make a guess at whether your patient come out on the better or worse end. A prognosis post is inthe works, but basically people with worse pain and more comorbidities, and people who’s pain is already becoming chronic, will probably do worse.

Most of all:

• Thanks for reading - but please don’t just read! What am I missing? What have I said that doesn’t fit your clinical experience, or your reading of the evidence? Please comment on this post, or reply to the email. This is too important for you to let me get away with my mistakes :)

Til next time,

Tom

P.S. a few test readers of this post asked for everything in visuals/charts. I’m happy to do that but would rather wait for criticism + corrections to come in first.

A couple of years ago I finished a rough-n-ready pdf book on sciatica called Sciatica: The Clinician’s Guide.

The book was really, really popular. It hit the sweet spot of illuminating so many confusing clinical presentatons (“Oh, that’s why that happens!”) while also just being a really good read.

And the reception to the book will always be one of the defining moments of my life. I couldn’t believe that not only were people buying it but they were also reading it - cover to cover! - and even recommending it to their friends.

I took the book off the market over a year ago because I knew it could be made even better. Prof. Annina Schmid agreed to help me with the task. We re-wrote every sentence, we re-drew every illustration and we designed a beautiful cover. Oh, and we gave it a new name - Understanding Sciatica.

And now it’s finished.

I think you’ll really like it!

If you want to understand sciatica - the anatomy, the nerve injury, the disc herniations - it should be exactly what you’re looking for. It’ll help everything to ‘click’ so that you know what you’re seeing in clinic. It’ll allow you to discuss this confusing condition with your patients and colleagues with confidence. Plus, it’s just a really good read.

Click this button to get your copy:

Get *Understanding Sciatica*

Til next time,

Tom

Here’s the cover, if you can ever call it that, for the first version of my book on sciatica:

To be honest, I’m pretty pleased it’s this boring. I could have spend weeks and months faffing with it, and with the contents too, but something told me I just needed to get it out there in the world.

Now though, I have spend a lot of time faffing with fastidiously improving the contents - every illustration, practically every sentence, all with Annina’s help - and turning it into a paperback, too… so it needs a beautiful cover. How to make one?

I start by hiring a designer on a website called Reedsy. I send the designer a brief. I try to explain that although the book is rigorously scientific, it is pretty informal and definitely not a textbook. (I end up giving what is probably a nightmare brief, to be honest. A lot of “it’s X, but it’s also, like… the opposite of X”. For example, “it’s serious and authoritative, but also fun and friendly.”)

I also gave her a few illustrations she might like to use, like this one:

A couple of weeks later, she sends me some first ideas:

Not bad! Professional looking. But they also feel bit too cold and clinical to me. They look like the covers of a book that’s going to hold the reader at arm’s length. And also, none of them really visually represent sciatica.

But I decide to go with it and ask her to make a few changes - can we see the whole figure rather than a close up? Can we highlight the affected nerves? etc. - and a couple more weeks later she sends me this:

Now, the visuals feel a bit more sciatica-y. It’s definitely good enough.

But the yellow highlighted nerve looks wispy and insubstantial. And I don’t love that blue. And once someone points out that the dartboard/target looking thing looks exactly the same as the neurofen logo, I can’t unsee that. So on the whole I’m not that excited about it….

Nevertheless, it is still good enough, and I have already peppered the designer with finicky requests for this change and that change, so I settle with what we have.

A year or so passes and the re-write is finally finished (the book has also been re-named). I go back to that design, and I still feel kind of deflated about it. I want the cover to just be a bit cooler. So I try to make my own…

I stick with that interesting old-fashioned image of the nervous system, and play around on Canva…

I manage to make something that is visually striking, and looks serious but also singular and characterful:

But it’s clearly made by an amateur, and I try as I might I can’t make it look any more professional. Plus, when I ask on twitter, a lot of people really hate it, saying it reminds them of fusty old uni textbooks (it’s meant to be retro, but apparently it’s too retro). Some people even DM to try to persuade me that it’s not good enough for the book!

Okay, okay. Forget designing it myself.

So, as if I am made of money, I simply hire another designer and start again.

I re-hire the designer who made the beautiful cover for Cauda Equina Syndrome: The MSK Clinician’s Guide - a process that went very smoothly.

I make the brief a bit less self-contradictory, and give the designer four or five very specific ideas (along the way I have learned that they don’t seem to actually want a blank slate, but would rather be pointed in a clear direction).

One of the ideas, which is what the designer decides to run with, is that we should flip this old modernist poster upside down, making it look like a cauda equina, and single out one of the roots somehow to imply it’s the ‘sciatica root’.

Here’s what the designer sends me:

Now already, this actually looks like a book one might like to read, so I’m happy. But the cauda equina is off at an odd angle (when would it ever be like that physiologically - during a handstand?) and the colour blue makes it look like a fountain. (Also… Annina’s name is wrong!)

I send back some notes and a few weeks later he sends back these:

Bold and beautiful! But still not quite right. The multi-coloured ones are great to look at, but it’s not obvious which root is ‘the one with sciatica’, so the whole visual metaphor is diluted. And I still don’t like that watery blue in the other one1.

But if we can fix the colours, we’ll be there. Rather than have a long back and forth with him about the endless colour combinations he could show me, I decide to do this myself. I like this green one until someone points out it looks like a Christmas tree:

Maybe this yellow one? But it looks a bit washed out…

Then, I think to change the background so it matches the background of the CES book…

And… that’s it! This, I like… I think it’s the first one in all this time I’ve actually liked looking at2. I haven’t tested it on twitter yet, partly because if people don’t like it I don’t have the heart (or cash) to start again, but mainly because even if a lot of people do dislike it, I don’t think I can be persuaded away from it. It’s memorable, bold and, if it’s to your taste, beautiful, without giving up any professional gravitas. And most of all, it clearly communicates that the book will not be boring.

So there you have it. Front cover done. Now i’m just waiting for the spine and back cover than then finally, at long last… it will exist in the real world.

Til next time,

Tom

P.S. I have chatted to a few people privately about the process of independently publishing a book - get in touch if you want to do the same.

In the meantime, I thought I’d re-send this podcast that Annina and I recorded in September 2020. It’s still the most popular episode of the pod. Might nerve pain be the most interesting thing in the world?

Below are the timestamps for the Q&A, with some relevant pictures and links. (Please by aware if you are reading this through your podcast app, the pictures and links may not show). If you have not heard from Annina before, I recommend her episode of The Physio Matters Podcast as a good introduction on this topic. Today’s podcast takes more of a deep dive!

Timestamps

0.00 - 2:55: intro

2:55: is radicular pain neuropathic?

I reference Annina and Brigitte Tampin's classification for low back related leg pain which you can see more about here

Annina mentions the NeuPSIG grading system for neuropathic pain:

6:48: ectopic activity from abnormal impulse generating sites 

Ectopic means "in the wrong place". Ectopic activity means action potentials arising from the wrong place in the nerve. For example, instead of arising in the peripheral terminals as they should, action potentials can be generated in the nerve trunk or the dorsal root ganglion. In entrapment neuropathies, this will typically happen when a patch of the nerve becomes demyelinated and ion channels lodge in that part of the cell membrane. This picture shows the process in a nerve that has been completely cut, but the concept is the same for nerves that are merely crowded out.

9:07: mechanisms of stress-induced radicular pain

I mention a paper by Elspeth McLachlan which found that after sciatic nerve ligation, noradrenergic axons in rats sprout into the dorsal root ganglion and form basket-like structures which can activate sensory neurons.

12:19: allodynia, wind up and other neuropathic pain features in radicular pain

14:55: reaction of dorsal root ganglion to nerve root injury

Dorsal root ganglion

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19:08: distal changes in radicular pain, loss of nerve fiber density

I mentioned a study by Andrasinova et al. that showed loss of intra-epidermal nerve fiber density in people with radiculopathy. This beautiful artwork by Kathleen Sluka shows intra-epidermal nerve fibers.

26:08: antidromic impulses

Antidromic impulses are action potentials that go "the wrong way". They are part of some normal physiological processes, I think, but when associated with pain and ectopic action potentials they are pathological.

One possible cause of antidromic impulses from dorsal root ganglion ectopia - pic from Sorkin et al.

28:48: why would nerve trunk blocks reduce nerve root pain?

I mentioned a paper from 1990 by Xavier et al. where they note that nerve blocks to the sciatic nerve trunk eases radicular pain, and suggest this might mean antidromic impulses are important for radicular pain. I also mentioned a study by North et al. that found nerve blocks distal to the nerve root ease pain.

Another interesting read is this paper from 1984 by Norden et al., who measured antidromic activity in the sural nerves of two people with radicular pain - activity that correlated with increases in symptoms.

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34:05: avoiding pain or pushing through the pain

37:33: can we determine the underlying mechanism of radicular pain clinically?

Annina mentions case studies from McKenzie practitioners who can reverse loss of function, like a foot drop, through repeated movements. She suggests this might be a sign of ischaemia. I have not been able to find a video of this. But on Mark Laslett's course he showed a video of one of his patients who developed myotomal weakness - unable to heel walk - when sitting slumped but recovered strength with repeated extension.

40:47: oedema as a cause of compression

43:17: surgery for longstanding radicular pain

46:06: Annina asks me why I'm so interested in sciatica!

49:30 - end: discussing the role of observation and creativity versus rigour and quantitative data in science

Understanding Sciatica, with contributions by Annina Schmid, will be published…. soon?

If you’re no longer interested in these, please scroll to the bottom of this email and click unsubscribe!

Hi everyone,

I was recently asked to compile a reading list on CES for the BritSpine conference. The full reading list is here. I thought it would also be fun to put together a ‘starter for 10’ list - if you’ve not delved into the literature on CES before, which ten papers should you start with?

First you want to get a handle on what CES actually is, beyond that list of red flags we can all repeat in our sleep!

For that, Fraser et al. (2009): Cauda Equina Syndrome: A Literature Review of Its Definition and Clinical Presentation gives some nice background about how this thing we call ‘CES’ has been described and defined over the years. And Lavy et al. (2021): Cauda equina syndrome—a practical guide to definition and classification puts a nice bow around it all, while also describing the all-important ‘stages’ of CES.

Next, you’ll want to know how to look out for CES in your practice. Of all the terrific papers by this research team, Assessment and management of cauda equina syndrome by Sue Greenhalgh and colleagues is probably the most comprehensive. Next, you’d do well to read two sets of guidlines, firstly The British Association of Spine Surgeons standards of care for cauda equina syndrome by Germon and colleagues (2015) and secondly Getting it Right First Time: National Suspected Cauda Equina Syndrome Pathway compiled by Mike Hutton and many others, and released just this year. Full disclosure, I haven’t read the latter myself yet, but it’s clearly going to be the North Star for practice for the next few years, in the UK at least.

Next, here’s a good high-level review: Gardner et al. (2011): Cauda equina syndrome: a review of the current clinical and medico-legal position. It includes a nice history of the debate about the timing of surgery (not many people know there was quite recently an argument that you could delay surgery even for acute CES).

Going back to that list of red flags we could all repeat in our sleep, Rob and I are always banging the drum about how important it is to know that you don’t need a ‘full house’ of red flags, that you just need one card; and that many of the red flags we look out for are in fact end-stage CES, when we should be aquianting ourselves with the earlier, more subtle symptoms. I think two good papers to help work out how CES actually presents are Angus et al. (2021): Determination of potential risk characteristics for cauda equina compression in emergency department patients presenting with atraumatic back pain: a 4-year retrospective cohort analysis and Woodfield et al. (2023): Presentation, management, and outcomes of cauda equina syndrome up to one year after surgery, using clinician and participant reporting: a multi-centre prospective cohort study. They’re similar; I reviewed them here.

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What happens to your patient in the emergency room? If they’re lucky, they get an and MRI; they might instead (or also) get a bladder scan and, if they’re unlucky, a digital rectal exam. What’s all that about? A good paper on the digital rectal exam, at least, is Tabrah et al. (2022): Can digital rectal examination be used to detect cauda equina compression in people presenting with acute cauda equina syndrome? A systematic review and meta-analysis.

Most people referred for an emergency assessment for CES don’t actually have it. To understand why someone might really, really seem like they have CES but have a pristine MRI scan, read Hoeritzauer et al. (2021): 'Scan-negative' cauda equina syndrome: what to do when there is no neurosurgical cause.

Finally, I’m a big fan of reading historical papers, which always give the best clinical descriptions and always seem to illuminate something elusive about a topic that modern papers just don’t. There are a few on CES, but a good one to start with is Shephard (1959): Diagnosis and Prognosis of Cauda Equina Syndrome Produced by Protrusion of Lumbar Disk (which I reviewed here).

And that makes 10! Note that you can click on the paper names to open a pdf…

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Again, the full reading list is here - I am happy to share any pdfs from that, too. Just reply to this email.

Til next time,

Tom

P.S. All this research and more is synthesised in our book, Cauda Equina Syndrome, The MSK Clinician’s Guide.

This will be familiar stuff to lots of readers, but I also know there are many newer subscribers who are wondering about it - and I don’t think I’ve ever actually written a blog that gets it all down in one place in a simple manner.

You can find the new post here. I’m hosting it off substack so it’s more ‘permanent’.

There’s also of course the classic, longer paper by Bogduk which covers this brilliantly, and might really be the best place to start if you have the time.

Thanks, til next time!

Tom

Beyond the tweets, memes and infographics, what do we actually know about the relationship between disc herniations and radicular pain? I went through all the evidence and drew some conclusions. Please do let me know if I’ve missed anything important!

Herniations and radicular pain

Asymptomatic disc herniations are common (except for extrusions).

It’s well-known that herniations are common in asymptomatic people. We all know the table…

The wrinkle is that this table only mentions disc protrusions. But asymptomatic disc extrusions are not that common1. According to a less-cited Brinjikji paper, only about 1.8% of asymptomatic people have a disc extrusion.

This fits with findings from a study by Suri and colleagues, who followed asymptomatic people and intermittently gave them an MRI to see what was going on. Only five of the 123 people got a disc extrusion, and all five of them also got radicular pain2.

It seems that asymptomatic extrusions aren't a big thing.

But I don’t want to overstate my case - asymptomatic herniations in general are still pretty common. As Brinjikji and colleagues report, 29% of asymptomatic people in their 20s have a disc protrusion, and this rate increases gradually through life, up to 43% of asymptomatic people in their 80s. 

How can you have an asymptomatic herniation? Lots of reasons3, but here's some:

• Some herniations are not near transiting nerve roots (for example upper lumbar protrusions, or central or far lateral protrusions).

• Some herniations are presumably not that chemically-active, so that even if they are close to a root they don’t irritate it.

• Some herniations develop very slowly, so that even if they do encroach on a nerve root the root has time to adapt.

• All the non-local, broader systemic factors that might make someone more or less predisposed to pain, such as their immunological profile. 

In any case, the conclusion of this section: disc herniations do not always come with pain.

Herniations are more common in people with radicular pain.

For example,

• In the review I mentioned above, Brinjikji and colleagues found that 1.8% of asymptomatic people had a disc extrusion, compared to 7.1% of symptomatic people. And 19% of people had a disc protrusion, compared to 42% of symptomatic people 4.

• Boos et al. found that 22% of asymptomatic people had herniation-induced nerve root compression (which was mostly minor), compared to 83% of people with radicular pain (which was mostly severe).

• Konstantinou et al. found that 32% of people with somatic referred pain had nerve root compression, mostly caused by disc herniation (some stenosis), compared to 60% of people with radicular pain.

• van Rijn et al. didn't compare symptomatic to asymptomatic people, but the symptomatic to the asymptomatic side of the spine in people with radicular pain. The asymptomatic side had a herniation 33% of the time, whereas the symptomatic side had a herniation 74% of the time.

In other words, people who have sciatica are, as you’d expect, more likely to have a disc herniation than people who don’t have sciatica.

The importance of disc herniations diminshes over time

For example,

• El Barzouhi et al. looked at the the MRI images of a group of patients one year after their treatment. They found that about a third of people who got better still had a disc herniation, and... about a third of people who didn't get better also still had a disc herniation. Another way of looking at the data: of all the people who still had a disc herniation a year after treatment, 85% felt better5.

• In a similar study, Barth et al. found that two years after surgery, many patients still had herniations (remnants and reherniations), but these findings didn't correlate with their clinical status.

• Fraser et al. found much the same thing, 10 years after treatment - "the presence or absence of herniation had no significant bearing on a successful outcome"

Essentially, after a year or so, most people's pain seems to be doing its own thing, irrespective of what the disc is doing! It seems that herniations are generally short- to medium-term trigger of radicular pain. Presumably they ‘spark’ the neural mechanisms of pain such as neuroinflammation, structural nerve damage, ectopic sites, and local scarring and tethering; and, once sparked, those mechanisms are partially self-sustaining.

Bonus ?fact: People with leg pain but no back pain might be more likely to have an extrusion than a protrusion

Just an aside based on two small studies:

• Pople and Griffith found that 96% (!) of people with sciatica but no back pain had a disc extrusion.

• Reihani-Kermani found that people with sciatica but no back pain were 6.5x more likely to have an extrusion. And, if their radicular pain increased as their back pain decreased, they were fully 10x more likely.

Now, let’s look at…

Herniation size and radicular pain

Herniation size is (probably) not associated with the degree of pain

For example,

• Dunsmuir, amongst 56 patients - "There is no direct correlation between the size or position of the disc prolapse and a patient’s symptoms".

• Karpinnen, amongst 160 patients - "Magnetic resonance imaging is unable to distinguish sciatic patients in terms of the severity of their symptoms"6.

• Mariajoseph, amongst 122 patients receiving a microdiscectomy - "Disc fragment weight had no effect on the severity of pain".

• Seo, amongst 43 patients undergoing conservative treatment - "No statistically significant correlation was evident between symptom severity and disc volume".

• Not quite the same thing, but related - Jensen et al. found that amongst patients with radiculopathy, nerve root touch caused as much leg pain as nerve root displacement or compression.

This appears to conflict somewhat with the fact that, as we’ve seen, extrusions (bigger) seem more likely to cause pain than protrusions (smaller). I think the thing is that once a herniation is painful, it doesn't much matter if it’s big or small.

(Of course, this is all just pain. Herniation size does seem to be associated with the degree of neurological deficit).

Herniation size is (probably) not associated with the eventual clinical outcome

For example,

• Gupta - "There is no statistical association between the size of a lumbar disc herniation and the likelihood that a patient will fail conservative treatment and ultimately require surgery".

• Masui - "Clinical outcome did not depend on the size of herniation" after seven years

• Modic, amongst 246 patients with acute radicular pain or back pain - "there was no relationship between herniation type, size, and behavior over time with outcome."

So, the size of the herniation doesn't seem to matter much.

That might be because of measurement problems when it comes to MRI (which, after all, is not the eye of God; and what would upright MRIs have found?).

But even accounting for measurement problems, it seems that size doesn’t matter much. Why not? Well, nerve roots are relatively fixed in place on the disc-side of the spinal canal, which means that a herniation doesn’t have to be particularly big to add significant mechanical pressure to a root anyway. And radicular pain is in large part driven by discogenic chemical irritation, which renders the actual size of the herniation less important.

So a disc herniation is not like a vice that causes pain through mechanical pressure, and causes more pain the more tightly it is wound. Considering the role of this chemical irritation, a closer analogy is that a herniation is like putting chilli powder on your fingertip and poking, or even just touching, your eye. The contact is important, and more pressure is surely not desirable, but the pain is mostly caused by chemical irritation.

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Change in herniation size is associated with a change in pain

As we know, herniations change in size over time, most of them shrinking as they are resorbed by the immune system, but some growing in size as more disc material escapes. And these changes in size do seem to go along with changes in pain. For example,

• Seo et al. split patients into a group whose herniations got smaller over time and a group whose herniations got bigger. Both groups' leg pain improved on average, but pain improved more quickly in the group whose herniations got smaller7.

• Ahn et al. found that a decrease in disc size of more than 20% correlated strongly with a positive outcome. 18 of 19 people whose discs decreased by 20% had relief of most or all of their pain.

• Fagerlund et al. found a "significant positive correlation between the improvement from sciatic pain and the reduction in the size of the individual hernia", amongst 30 patients

• Kesikburun et al. found that patients whose discs completely resorbed also had less pain, whereas patients with partial or no resorbtion did not, amongst 40 patients

• Komori et al. found that change in herniation size "mainly corresponded to clinical outcomes but tended to lag behind improvement of leg pain", amongst 77 patients. The lag suggests that the two might not actually be closely related; discs resorb and people get better but the resorbtion might not be the cause of the improvement.

There are exceptions, but it seems to be a trend that a change in disc size is associated with a change in pain.

It seems kind of contradictory that the size of a herniation isn't associated with pain, but change in size over time is. Maybe it's not the shrinking per se that causes a pain reduction, but the fact that a shrinking disc is also resolving as a biochemical event - fizzling out, becoming less inflamed... To put it another way, 'change in herniation size' might be a proxy for 'inflammatory process doing its thing, body working its way back to normal'.

Of course, by now we are looking at a lot of quite small studies, with inherent measurement errors, so I’ve got to be careful that I’m not just reading tea leaves. All conclusions about herniation size are tentative.

General conclusions

Although asymptomatic herniations are common, asymptomatic extrusions are not that common. And, as expected, people with radicular pain have more herniations than people who don’t have radicular pain. That said, the importance of symptomatic herniations decreases over time, because herniations are generally a short- to medium-term trigger for radicular pain. [EDIT: ‘Spark’ or ‘catalyst’ are good analogies; ‘kindling’ is probably even better].

Once a herniation is painful, it’s not necessarily the case that a bigger herniation is more painful, or vice versa. A bigger herniations also doesn’t mean a worse outcome in the long run. That said, as herniations get smaller people do seem to feel less pain.

That’s it!

It strikes me that the middle ground is a good place to be on this one…

As I say, please let me know if you think I’ve missed anything important.

Til next time,

Tom

P.S. Work on the republication of Sciatica Book 1 (now retitled ‘Understanding Sciatica’) continues! Nearly there… Here’s some of the pictures and here’s the work in progress cover.

Let's look at new two papers and one new book to see what we can learn about how CES presents.

Presentation, management, and outcomes of cauda equina syndrome up to one year after surgery by Woodfield et al., 2023.

For this study, Woodfield and colleagues collected data from 33 emergency spinal surgery centres across the UK, finding 621 people with discogenic CES.

How did these patients present?

Pain:

• 96% had back pain and 93% had sciatica. In other words, practically everybody with CES has leg pain and back pain - but not everybody! And a few people had pain that was relatively mild:

  

• Of all the people with sciatica, only about half of them had the red flag of bilateral sciatica. In other words, contrary to what you might expect, half of people with CES actually have unilateral sciatica.

Radiculopathy:

• 61% of people with CES had leg weakness and 77% had leg numbness.

• As expected, radiculopathy affected the lower lumbar nerve roots more than the upper: ankle dorsiflexion and plantarflexion, L5 and S1 dermatomes, achilles reflex.

Bladder dysfunction:

• 83% of people had bladder dysfunction.

• 41% of people had retention and 40% had incontinence - we can put these people at the 'end stage' of CES, where the bladder has shut down and begun to overflow.

• 22% of people had altered sensation and 37% a poor stream - we can put these people in the 'incomplete' stage of CES, where the bladder is still doing something but sensory and motor function is impaired. A reminder that bladder dysfunction in CES is not just about incontinence.

• Another way of looking at this is that 20% of people with CES do not have bladder dysfunction. So, just because someone doesn't have any bladder changes, doesn't mean they can’t have CES.

Loss of saddle sensation:

• 81% of people.

• Many of these people had unilateral loss only.

Bowel dysfunction:

• 39% of people. Fewer than had bladder dysfunction or a loss of saddle sensation. This chimes with previous studies.
  Why is bowel dysfunction less common? Partly because just use their bowel less often, so they don't notice a loss of function. On top of that, the bowel takes longer to back up and overflow than the bladder, so bowel incontinence doesn't usually occur as soon as bladder incontinence.

Sexual dysfunction:

• 38% of people.
  In all studies like this, sexual dysfunction is the least common red flag. Why? It might be partly because sexual function is less affected than bladder function and saddle sensation. But it's also surely because most people with CES aren't trying to have sex or masturbate, and also because those that are might be reluctant to report any loss of function. And, clinicians aren't asking about it as often as they should, so it doesn’t get reported.

• Of people with sexual dysfunction, 63% had difficulty achieving an erection or orgasm, and 40% had a loss of sensation.

A few more notes from this study:

• The average age of a person with CES was 42. This is also the average age of... people in the UK! Nevertheless, that's some evidence for the idea that CES happens in people who are young enough to still have a well-hydrated disc capable of generating the outward pressure to herniate, but old enough to have some weakening in the annular wall to allow that herniation through.

• 59% of people with CES were able to empty their bladder pretty well. More evidence that bladder scans are not a replacement for MRI. Sadly, it's not too reassuring when your patient is sent home from A&E because their bladder scan was normal.

• The authors tried to divide CES into stages - early, suspected, incomplete and retention - but found that clinicians couldn't agree on them so they had to abandon the idea. These stages seem very useful for understanding CES on a theoretical level, and result in many a 'oh, I get it now' moment; but they don't seem that useful or reliable IRL. I believe they are being dropped from the upcoming GIRFT guidance.

• The authors managed to cover every single A&E department in Scotland (!!) which meant they could reasonably assume they'd caught every case of CES in that country during the time period studied. They worked out the incidence as 2.7 cases of CES per 100,000 people per year. This confirms my suspicion that CES, though rare, is not nearly as rare as some people make out (can we stop quoting made up facts, now?)

There is much more in this fantastic study by Woodfield and colleagues, for example on the long-term outcomes of CES and the timing of surgery - but I won't go into it all here.

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Determination of potential risk characteristics for cauda equina compression in emergency department patients by Angus et al., 2021.

Let's look now at another recent study by (previous podcast guest Michelle) Angus and colleagues. This was a retrospective notes review that identified 111 patients with cauda equina compression. (It's worth saying what an amazing achievement it is for the authors of this study and the previous one to get data on so many patients - even the biggest previous studies have only a few dozen patients).

What do we learn from this paper?

Firstly, when it comes to how CES presents, Angus and colleagues' results are quite similar to Woodfield and colleagues'. The age of patients was about the same, 46. Practically everyone with CES had back or leg pain, but not quite everyone. Bladder and saddle problems were the most common red flag symptoms; bowel and sexual problems, the least1.

The extra neat thing in this study is that Angus and colleagues compared all these people with CES and MRI-confirmed compression of the cauda equina to all the 888 people who came in to the emergency department suspected of having CES but who turned out to have no compression of the cauda equina on MRI2.

In other words, Angus and colleagues looked at this huge group of patients suspected of having CES, divided them into the 111 of whom did and 888 of whom didn’t, and asked… what's the difference?

Not much! For example, here is the graph comparing sensory changes in the saddle, genitals, bladder and legs. Blue = people with CES; orange = people with no CES. The bars are pretty much the same height: in patients with and without CES, the rate of sensory changes is about the same.

So too for the other red flags. Urinary incontinence, faecal incontinence, sexual dysfunction: they all occur at pretty much the same rate in people who have cauda equina compression and people who just look like they have. The same is true for the clinical tests administered in A&E, the bladder scan (again) and the digital rectal examination (which latter mirrors a recent paper by Tabrah and colleagues).

If you’d asked me before reading this study, I think I would have expected more differences than this. It’s true that in one sense you would expect CES and not-actually-CES to look similar; after all, the people with not-actually-CES have been referred to the ED because they… look like they have CES. But it’s also really quite surprising that, say, fully 31% of people with not-actually-CES have a loss of anal tone, and by contrast that only 35% of people who do have CES have a loss of anal tone.

But it’s not all null null null. There were some features that indicated someone was more likely to actually have cauda equina compression on their MRI. Those features were:

• Bilateral leg pain,

• Objective sensory loss (in a dermatomal distribution), and

• Bilateral ankle reflex loss, especially if also bilateral knee reflex loss.

Notably these are all features of a painful radiculopathy. Maybe they filter out the people who only seem like they have CES because they are having a kind of panic or shock reaction to severe back pain, causing bladder dysfunction and functional weakness. Such people have pain and weakness but are less likely to have the particular signs and symptoms associated with an actual radiculopathy3.

In any case, Angus and colleagues are careful not to say they have discovered a special test we should all be using in clinic tomorrow - this is more information to inform further research and clinical reasoning more broadly.

The Lost Tribe, Various Authors.

So far, so many statistics. A new book written by people with CES will give us some colour. The Lost Tribe is published by the CES Champions charity. Each chapter is a different CES story, written by someone with CES.

Let’s look at a few stories from the book to see how CES might first manifest.

In one chapter, Claire explains that although she had always had grumbling back pain, the first symptom of CES was "strange sensations in my genitals". It wasn't until some time later that she had a more typical, dramatic event:

"I turned over in bed one night and suddenly this back pain gripped me, so vice-like I could hardly breathe [...] and then I became aware of pins and needles in my buttocks. It felt as if I had enormous weights strapped to each one, as if all the muscle tone had disappeared".

It's worth noting that 'pins and needles and heaviness in buttocks’ isn't explicitly a red flag for CES, although it does make perfect sense if you know how nerve root injuries work. (Another writer says "I had a horrible sense of everything drooping...")

In another chapter, Laura tells us a very different story:

"I was just sitting at my desk at work, when the toes in my left foot went numb. I shifted about and loosened my boot, thinking my footwear was just too tight [...] But that didn't help. As the morning wore on, the numbness started to spread from my big toe along to my other toes and across my foot. I took my boot off and moved my foot about to try and get the feeling back into it, as you do with pins and needles, but that didn't help either."

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In another, Duncan, writes that

"One Monday morning I woke up in Bristol, and I couldn't get out of bed. I called the doctor in a panic. [After an epidural, the third in the last few years] I chose not to go home and be alone. There was something about the pain that was so unusual. I knew it wasn't right.
Luckily, my great friend Tara Palmer-Tomkinson [did I mention this is Duncan from Blue?] lived on Earls Court Road, just around the corner from the hospital, so I called her up and asked if I could stay with her for the night. [...] 'You know what you need, darling', she said in true Tara style, ‘a shot of vodka. That will sort you out.’ [...]
That night I could feel my left leg going numb, so I frantically messaged my doctor telling him this, to which he replied 'Don't worry, it's just the strength of the epidural. Give it a bit more time and everything will be fine. Tara gave me a sleeping pill to compliment the vodka and I managed to knock myself out until eight in the morning when I woke up dying for a wee. But I couldn't go. No matter how hard and how often I tried, nothing would come out.”

This book also has some very useful descriptions of red flags symptoms.

For example, here are some descriptions of bladder dysfunction:

• “Like trying to pee through a straw" (Claire).

• "It became more difficult to urinate. I would have to sit on the toilet and force it out" (James).

• "As I was walking to the car, I was suddenly aware that I'd wet myself [...] 'What is going on?' I thought to myself" (Steven).

And some descriptions of some other red flags:

• Bowel dysfunction is the "awful feeling of having a football eternally stuck up your arse", says Martin (who clearly still has the sense of rectal fullness that often goes missing with CES, despite his bowel retention).

• One lady says of the sexual dysfunction that "If I shut my eyes and slept with the entire football team, I would be unaware of it".

• On the pain: "I feel as if I've been dropped by a helicopter from a great height onto a telegraph pole with a pineapple strapped to the top of it". (Why do we not often talk about saddle and rectal pain with CES?)

Another thing I noticed in the book was that almost every single writer had long term back problems before developing CES. (The one exception was the writer who developed CES after giving birth, likely related to her epidural). This should put paid to the idea, that I do think is floating around out there, that CES is an acute condition that comes out of the blue and, by extension, that if someone's doesn't have CES on initial presentation then they're 'in the clear'. Disc herniations are not all-or-nothings, but ongoing events.

So keep asking, and keep educating!

This book certainly helps us to understand the importance of asking and educating patients about CES. Many of the writers describe being confused about the onset of their symptoms, not even aware that they were related to the spine, never mind something called cauda equina syndrome. "I was baffled", says one; "I couldn't explain what it was", says another. And another: "This was very weird. My left leg was completely numb and now I'd lost my ability to pee. Were the two things connected?"

In one story, James recalls that an ambulance crew came out to see him after a flare up of his long term spinal pain. They gave him gas and air and helped him get to bed, saying he didn't need to see anyone that night. "Kate [James's partner] looked doubtful, but they were medical professionals, so I didn't think to question their approach. When I woke up in the morning, the first thing I noticed was that I had wet the bed. I put it down to the fact that I was off my head on gas and air last night." James would wait another week for surgery. One senses that with just a bit more knowledge, with even just the magic words 'cauda equina syndrome', this story might have been different.

Oh, and it’s not just our patients who need to know more about CES - far from it! This book has many frustrating episodes of clinician ignorance... But let’s finish on a good note - of her GP, Claire writes,

"I owe a debt of gratitude to my own GP, Dr. White. If he hadn't taken the time to ring me at the end of his working day, to see how I was after being rebuffed at A&E, I have no doubt in my mind I would be in a wheelchair right now [...] Thank you, Dr White, I am eternally grateful."

If you take a particular interest in spinal stuff and you want to add another layer to your CES knowledge, I recommend buying The Lost Tribe (Amazon link here). There’s much more to it than what I’ve quoted, particularly around the long term story of CES and how it affects people’s lives. It’s not expensive and all the money goes to a good cause!

Wrapping up

So, three new publications, lots of new data and new stories. Thanks to the authors of these fantastic publications for all their hard work and talent.

There’s too much here to sum up neatly, but here are some final reflections:

• CES has a classic picture, of back pain with painful radiculopathy plus bladder dysfunction and loss of saddle sensation. Typically, bowel and sexual dysfunction come later, if at all.

• There is a lot of variation around that classic picture.

• For example, no one red flag symptom must be present. Not everyone with CES has bladder dysfunction, for example, and a few people with CES people don’t even have back pain!

• And, many early symptoms of CES don’t fit the classic picture. Many people with CES are not incontinent and can empty their bladder properly, but have, for example, a poor flow.

• Another source of variation in CES is how individual patients experience it and describe it - after all, it’s a bio-psycho-social condition like any other.

• Lots of people who don’t have CES really, really look like they do!

• One implication of all this is that we should be aggressively un-learning the tick-box approach to CES and trying to develop pattern recognition about what it actually looks like, how it unfolds over time, and how patients describe it… then reasoning it through properly, educating and involving our patients as we go! (There’s a book for that 😎)

Til next time,

Tom

Happy new year! Let’s look back at the third year of this newsletter.

The good

• Rob and I published our book Cauda Equina Syndrome, The Clinician’s Guide, which has sold well and received really good feedback.
  
  I’m very satisfied with the book because I think we achieved a very specific and ambitious goal, which was to make it useful, singular and interesting to read. This is in contrast to so many clinicial books which are theoretical, generic, and boring. What’s more, a lot of the feedback we’ve got for the book confirms that we achieved this: people frequently say there’s just nothing else like our book out there, and that includes other stuff on red flags and CES.
  
  Another big step forward I’ve made with this book is that it is an actual book, printed and bound and existing in the real world with a lovely cover. This was a lot of work compared to my previous book which was really just a pdf. It took a long time to find out how to make a paperback of reasonable quality without it costing an arm and a leg to print. Now that I know how to do this, it should be a lot less work next time.

  

• The most popular email this year was the print-it-yourself sciatica zine. It was fun to make this (at least, after a few inevitable ‘forgot to click save and lost everything’ episodes) and I think it’s something genuinely different and interesting. The zine format is a good way to do what I enjoy and am good at: distilling a lot of research into something quite straightforward, without losing any nuance, and without being too serious about it. The second zine, on assessment, I priced at five dollars - it sold very well.

  

• Another popular email was ‘On Being Wrong’ - it’s encouraging to know that I can write about stuff that isn’t sciatica and people still like it!

• More of you keep subscribing! Happily, this is without me having to do too much self-promotion on twitter etc. - so, thank you if you’ve shared and recommended it this year.

  

The bad

• This year, no email reached the dizzy heights of what I now think of as the ‘classic’ posts of 2020 and 2021!

  
  I don’t feel too bad about this though, as it’s pretty much a result of having far less time to spend writing, now that we have two children. The time I do have, I have to spend on stuff that will more directly generate income, which isn’t newsletters, sadly. So there have been fewer really high quality emails this year.
  
  

• The CES book sold well, but it didn’t sell as quickly as my first sciatica book. I put this down to a few factors: 1) it’s a slightly more niche topic; 2) we published it at the height of the cost of living crisis in the UK; 3) I didn’t have time to dedicate to promotions and podcasts etc.; and 4) we haven’t made an ebook version yet, which means once you include postage and packaging the paperback costs about thirty pounds (we can’t make it cheaper due to the printing cost). We’re aiming for the ebook to be out in the Spring and we can price this lower.
  

• I didn’t achieve last year’s goal of re-publishing my sciatica book. I took it off the market over a year ago, I think, with the aim of re-writing it, re-illustrating it, and making it available in paperback. I’m pleased to say I have done much of this work… practically every paragraph, maybe every sentence, I’ve improved in some way, and 80% of the illustrations too.
  
  But I don’t feel too bad that I haven’t quite finished yet, because the main reason is that I’ve been collaborating in this work with the amazing Annina Schmid - and although collaboration takes longer, it has improved the book substantially.
  
  [As a reminder, if you did buy the original version of this book I will be emailing you when the re-write is out to let you know of significant changes, major and minor - none of that ‘you have to buy the second edition to find out what’s changed’ malarkey!]

Life news, and what’s next in 2023

Of course the biggest thing to happen in 2023 was the birth of our second child, baby Eve. She’s just over two months old now. She has had some quite serious health problems which we’re still trying to get to the bottom of (I’m writing this from her hospital room). I feel so fortunate to have Eve in my life. She’s lying next to me wiggling away as I type this.

You might know that we live in Houston at the moment, where my wife has recently finished a postdoc. We’re staying in Houston for the time being as she has been offered a position to continue at the same place, and we like it here. It’s ridiculously hot and humid and much uglier than our previous home in Michigan, but apart from that life in Houston is very good, and it’s a good place to raise a family!

So what’s next for the sciatica newsletter, and my work on sciatica more generally?

1. Re-publish my previous book on mechanisms of sciatica and disc herniation.

2. Publish the ebook of the CES book.

3. Publish another zine or two.

4. Encourage other clinicians to write. With a few important exceptions, clinical writing has now become polarised between twitter threads and doorstop textbooks. Both great, but severely limited. There is so much tacit knowledge out there we need to unlock, which means writing proper stuff! I want to help people do this. (I have some ideas about how… Do get in touch if you’re interested).

After those four things… I have to think very carefully.

One of my big goals with the newsletter has long been to write a book on the treatment/management of sciatica. When I started out, this was realistic. And indeed, I did write two other books! Now, however, this is a lot less realistic. We have two young children, which means it’s nearly impossible to put in the sustained time and focus required to research and write a high quality book.

It’s a shame because I have so many great ideas! And I think the book does need to exist, too.

I don’t want all this to sound too final - there’s lots of interesting and important work to be done to help clinicians and theur patients with sciatica. I just need to think hard about whether a book is the right thing to do, for me. And if it is, how do I make it work with my other responsibilities?

Do let me know your thoughts and impressions of what I’m saying here - I’m curious.

Well that’s it. Here’s to another year of learning, writing and drawing! Til next time,

Tom

With a newborn to look after, it’s been very hard to do any new research or writing. So, for this edition, I’ve improved and updated an old post from elsewhere.

This piece is for non-clincians. Do print and share it with your patients!

Exercising When It Hurts

This post is for people who have muscle, joint and/or nerve pain that has gone on for a long time and doesn’t seem to be going away. It is meant to help you to become more fit and active, so that your body and mind are as healthy, happy and capable as they can be, despite your pain.

Why exercise?

We are always being told about the benefits of exercise. For example, improved cardiovascular health, stronger bones and muscles, lower rates of depression, longer life expectancy, and so on. I prefer to think of the benefits as more individual to each person. Perhaps it means you are able to go to the shops without needing help, pick up your grandchildren without fear, or do a shift at work without feeling exhausted at the end of the day. In other words, exercise increases your capacity to do things that are important to you.

Step 1: Ask The Key Question

I encourage everyone to visit a doctor or physiotherapist and ask The Key Question:

“Am I safe to move?”

Usually we ask a medical professional for a diagnosis, medications or advice about the best treatment. It is important that you do that, but I’m assuming that people who are reading this post already have, and are still in pain and not where they want to be.

To exercise, what you want to know from your doctor or physiotherapist is whether you have a condition that means you should avoid exercise and movement. There are really surprisingly few of these.

In fact, for most muscle, joint and nerve pain, exercise is not only safe but strongly recommended by health professionals. This includes joint pain like hip and knee arthritis, and neck and back pain, including spondylosis, sciatica and disc problems.

Step 2: Understand that “hurt doesn’t necessarily equal harm”

For most of our lives, pain is a useful thing that protects our body. If I touch a hot stove, I feel pain and I quickly withdraw my hand. Pain is like an alarm that warns me of danger.

Unfortunately, persistent pain is much less useful. It is often well out of proportion to any damage going on in the body, and people can feel terrible pain when moving even when it is not dangerous. The alarm that is usually so useful can become “over-protective”.

This means that if there is a particular movement you do that causes you pain, and has done for some time, it is quite possible that the pain is not indicating you are doing any harm. In other words, you are sore, but safe. This is important to understand because otherwise the idea of exercising makes no sense, and you will just be miserable!

Another way to think of this is like a lowering of the pain threshold. A certain part of the body - or many parts - becomes over-sensitive to movement and feels more painful than it needs to be.

This is why step 1 is seeing your doctor or physio and asking, “Am I safe to move?”. You are asking a professional whether you are sore and need to rest, or sore but safe to move.

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Step 3: Decide which exercise

The best exercise is one you enjoy, because you’re more likely to stick to it. So, think about something you’ve liked in the past or something you’ve always wanted to try. If you’ve never enjoyed exercise and it’s just not your thing, try to recall a time when even if you didn’t like the exercise it at least made you feel a bit better after!

Exercise doesn’t have to be a sport or the gym. For our purposes, exercise is anything that’s more demanding than your usual day to day life. For some people, this could be walking, swimming, dancing, lifting and carrying...

Preferably, whatever you’re doing should make you feel a bit out of breath, sweat a little, or make your muscles feel tired. That said, this might not be possible if you’re starting from a low level or your pain is particularly bad.

Avoid the trap of choosing something you think you “should” do. If you have back pain, you don’t have to do pilates. If you have knee pain, don’t think you have to do exercise in the swimming pool. They are both good options, but only if you actually want to do them.

Make sure there is going to be as little “resistance” as possible to your choice. If you choose to go swimming regularly with a friend but the pool is a long drive away and your friend is very busy and likely to cancel, you might be setting yourself up for failure. On the other hand, if the pool is near your house and your friend is reliable, that would be a perfect situation. So, try to choose something that will fit in as easily as possible with your existing routine.

Here’s some ideas:

• Walking

• Running, for example Couch to 5k or Parkrun

• Cycling or an exercise bike

• Lifting weights at the gym

• Walking up and down the stairs

• Carrying heavy bags

• Racquet sports

• Dance classes

• Gardening

• Home stretches or yoga

• Exercise class at your local health centre

• Rock climbing

• Escape Pain app or local class

• Youtube/DVD workouts, or NHS fitness studio

• Youtube/DVD dance tutorials

• Home strength exercises

For more tips about approaching exercise I recommend this great list of “common sense exercise and movement guidelines”.

Step 4: Get started and get into the swing of it

When you have decided what you want to do, decide when you want to do it. Aim for three or four times per week. More than that is okay if the exercise is quite easy. But if you are working hard it is often best to give your body a day off in between workouts so it has time to recover and adapt.

When you know what you want to do and when you want to do it… do it! And for now, don’t worry about anything more than just doing it. The details don’t matter; keep it simple at this stage. The key is to “just show up” - at the gym, in the park, in front of your TV with an exercise DVD on, or wherever. Build the habit.

Explore the movements involved in whatever you are doing. Get used to how your body feels, see how it reacts, see how your pain reacts. Be curious about moving your body. Don’t feel you have to work yourself to exhaustion.

If you miss a workout, don’t beat yourself up. Just try again next time.

What about the pain? The golden rule

On the one hand, we know that pain can be like an “over-sensitive alarm” and doesn’t necessarily mean you are doing damage, which means you don’t need to avoid pain (assuming your doctor or physio or chiropractor has confirmed this). And, some pain - or at least discomfort - might even be necessary to get a good workout. But, you don’t want too much pain because pain… is still pain! Especially nasty is the kind of pain that ‘flares up’ after exercise and stops you from working and sleeping properly.

To solve this conundrum, I recommend sticking to the golden rule of exercise and pain. The golden rule is this:

Exercise within tolerable pain, that plateaus during exercise and does not continue to rise significantly, and gradually decreases once you have finished.

[If you’re curious about the research behind this ‘golden rule’, please see here, here, here and here.]

“Tolerable pain” is a funny phrase. It’s very individual. For some it will be a mild discomfort, for others it will be more. Another way of thinking of tolerable pain is that it’s ‘something you can cope with and feel is manageable’. It should not feel frightening and you should feel in control.

It will take some trial and error to find this level. At first, you might do too much and flare up your pain. Take time to let it ease off then try again, doing a little less. Think of a flare up as part of the learning process - you now know what is “too much” for you, at the moment. As you continue to exercise, it is likely that what was once too much will become achievable.

Be ready for DOMS!

Everyone, regardless of whether they have a painful condition, is likely to feel sore for the next day or two after trying something new. This is called DOMS - Delayed Onset Muscle Soreness. So, if you do feel worse after your first session, consider that this might not be a flare up of ‘your’ pain but normal muscle soreness that will diminish over time.

Congratulations!

If you’ve got started and got into the swing of it, you’ve made a huge (and hopefully enjoyable) positive change.

Stages 4 and 5 are about doing more, on top of what you’re already doing. These are optimal for fitness, but they’re not necessary for the good life. In other words, you don’t really have to do them. If you’re up and moving and a bit out of breath most days of the week, things are looking good. A little goes a long way!

If you do want to go a bit further, read on…

Step 5: Push on for more benefit

Once you have had a few weeks in a row of “showing up” and doing your exercises, no matter how little, and you have worked out the Golden Rule, it is time to start pushing on to get the most benefit from your time and effort that you can.

[Please note that there are some conditions like Long Covid and Chronic Fatigue Syndrome where ‘pushing on’ and doing more exercise over time is sometimes not possible. Please speak to your doctor about this, it is not my area of expertise.]

Once you are in the habit of exercise, you might find that you end up doing the same thing each time. For example, walking the same route, lifting the same weights, dancing along to the same DVDs. This is great and should be seen as a huge achievement! You could stop here, especially if you’re enjoying it. Or, you could try to do something more or something different. Getting out of your “comfort zone”, a little bit at a time, will help you to get the most from your exercise.

For example, try to walk a bit further, or do the same distance in a shorter time. If you are doing home exercise or weights at the gym, try to do a few more “repetitions” or lift heavier weights.

Give yourself some tough love. Are you out of breath? Sweating? Are your muscles tired? If not, you may not be getting the benefit you want.

Earlier, I said the best exercise is one that you enjoy, because you will stick to it. This is true, but it is also true that part of your exercise should be quite hard. Now, I’m not saying is that you have to Be Totally Extreme or ‘leave it all in the gym’. But every now and then you should challenge yourself to do a bit more than you’re used to.

A good rule of thumb is:

“What doesn’t challenge you, won’t change you”.

Step 6 and beyond: becoming an exercise expert

By now, your confidence will be high. It’s time to try new things. For example, if you mostly do things like walking and swimming, you would benefit from adding in some strength training - shorter, more difficult movements often using weights. It’s good to have a variety of endurance, strengthening and mobility exercises, if you can.

It might even be a good idea to flip the “best exercise is the one you enjoy” rule and actively try things that you are worried about. If you are worried about something then it is likely a weakness of yours that you might benefit from confronting. You might surprise yourself!

That concludes my six step guide to exercising when it hurts. It can be a tough road, with setbacks along the way, but it’s always worth it!

Finally, here’s a little poster made by one of my patients who benefited from this approach :)