Эпизоды
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We’re still working on the cover design for our upcoming book Understanding Sciatica - a frustratingly long back-and-forth process with the designer that I wish I’d started much earlier…
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
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.
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?
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Thanks for reading the 38th edition of my newsletter. This newsletter tracks my research as I write a book about lumbar radicular pain!
EDIT - The sound quality of this podcast is quite poor - you have been warned. I will try to transcribe it one day.
This edition, it’s my pleasure to bring you my conversation with Ash, a project manager from Chennai, India, who has a long history of back pain and sciatica but has nevertheless pursued his powerlifting goals and, to a great extent, recovered from pain.
Ash is deeply insightful about his journey and about his pain. During our conversation, he told me not only about how he approaches training with pain, both practically and psychologically, but also how he has found that things like sleep, stress, work and friendship all have a bearing on how his back pain and sciatica feel.
One thing that struck me during our conversation was how much work Ash has put in to teaching himself about pain and exercise. He showed me piles of notebooks and, on his laptop, reams of pdfs. He’s a skilled and tenacious autodidact. This is greatly to his credit, but it did also serve as a reminder to me of how hard it is for all of us - laypeople and clinicians - to get our heads round this pain thing.
I think this episode will be useful for clinicians who want a reminder of the power of education and of the right approach to training. I also think that, like my conversations with triathlete Kate Charlton (here and here), this episode will be useful for athletes with sciatica who want to get back to training.
Finally, here are some links to the resources Ash mentions during our conversation (asterisk = particularly strong endorsement from Ash):
* The Gift of Injury book by McGill and Carroll
* *Austin Baraki lecture
* *Explain Pain book
* *Barbell Medicine
* *Recovery Strategies by Greg Lehman
* Muscle Strength Pyramid approach
* Stronger by Science website
* Strength System, biopsychosocially enlightened gym in Chennai
* Back Pain talk by Mark Rippetoe
* *Aches and Pains article by Austin Baraki
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Пропущенные эпизоды?
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Thanks for reading the 31st edition of my sciatica newsletter. This newsletter tracks my research as I write a book about lumbar radicular pain!
Hi from San Jose, California, where I’m visiting the in-laws!
Here’s part two of my chat with Adam Dobson, where we discuss neuropathic pain, nerve assessment, exercise and rehab for sciatica, and more! Find part 1 here.
And here’s a few links to stuff Adam mentioned during our conversation:
* The IASP grading system for neuropathic pain
* The work of Dilley and Bove
* This trial by Mathieson and colleagues
* My newsletter on dermatomes
* Kerezoudis on the effect of epidural steroid injections on bone mineral density
* Adam’s bengal cat
I hope you enjoy our conversation - let me know what you think! You can contact me by replying to this email.
Lastly, a quick reminder of the free sciatica email mini-course, which is for anyone who wants to get up to scratch on the basics!
Til next time,
Tom
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Thanks for reading the 30th edition of my sciatica newsletter. This newsletter tracks my research as I write a book about lumbar radicular pain!
I must say things have been pretty quiet on the book front this week! In the time I’ve had to work on it, I’ve mostly just been wading through the literature. It seems like on any topic there’s really only a few key papers that give you most of what you need. But you have to read all of them to find out which are the key ones! It’s slow going at times…
Anyway, this week I want to share with you a podcast I recorded with Adam Dobson, a physiotherapist from the North of England with a keen interest in spinal pain (and author of this patient info leaflet).
I would describe Adam’s approach to assessment and treatment as pragmatic and sensible!
I think our conversation will be particularly interesting for people who are used to assessing and treating people with low back related leg pain, and know a bit about the basics of radicular pain, but still feel like they’re trying to put the pieces together to come up with an approach that works for them and their patients.
This first podcast, part one of two, focuses on assessment including referred pain, vascular masqueraders and other peripheral neuropathies!
At the end of this email, I have put some links to some of the papers and resources that Adam mentions.
Lastly I just want to say a huge thank you to Adam, not only for taking the time to talk but also for putting himself out there to talk about his practice!
Til next time!
Tom
Papers and resources mentioned in this podcast:
* Adam refers to Schmid and Tampin’s schema for understanding low-back related leg pain
* Here’s Adams extension of that schema, where he’s cast the net a bit wider (if this is too small, click here to see a bigger version)
* Here’s Adam’s summary of the ABPI test
* On referred pain, Adam mentions Kellgren, McCall on facet pain, and Lesher on hip pain.
* On entrapment neuropathies, Bowley and Doughty
* The BMJ paper and infographic on peripheral artery disease
* Mathieson on pregabalin
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Thanks for reading the 25th edition of my sciatica newsletter. This newsletter tracks my research as I write a book about lumbar radicular pain!
This week I spoke to Kate Charlton again! When we spoke last year, she was recovering from her second bout of radicular pain, getting back into her training and everything was going well. Since then, Kate’s pain returned. She chose to have surgery and so far, her recovery is going really well.
In the podcast, we talk about:
* Her decision to have surgery
* Returning to training after surgery
* Attitude and mindset
* And much more!
And, after last week’s newsletter, it was interesting to hear that Kate’s cold foot recovered immediately after her operation!
This conversation, and our previous one, will be useful for any of your patients who have radicular pain and want to return to sport, especially if they train and compete at a high level.
That’s it for this week! With a deadline looming, I’ve got to get back to work!
Til next time,
Tom
P.S. Here are some photos of some mourning doves that have started visiting our balcony. I’ve given them some seeds.
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Thanks for reading the 19th edition of my sciatica newsletter. This newsletter tracks my research into all things lumbar radicular pain!
This week I spoke to Professor Raymond Ostelo!
Raymond recently published a fantastic review of the evidence behind the treatment options for sciatica (link should be open access). In our conversation, we talk about the evidence behind the conclusions of his review. I ask Raymond about:
* How much confidence we should have in the evidence around sciatica
* Whether our research methods are sensitive enough to pick up on differences between treatments
* How clinical expertise fits in with evidence based practice
* What study he would conduct if money and recruitment were no object!
* How he thinks two trials he has been involved in - those lead by van Helvoirt and Luijsterburg - should inform our practice
* And more!
I hope you enjoy the podcast.
Other bits and bobs
* I recommend the latest episode of The Back Pain Podcast, a conversation with David Poulter about discs. He describes disc material as being like crab meat with added water…
* I learned a lot from the conversation under this tweet by Luke Murray, asking for advice for his friend with severe acute radicular pain. Here’s some highlights:
It strikes me that a lot of the options for Luke’s friend are based on no research evidence or poor research evidence. In fact, there is high level evidence that says that oral steroids, anti-neuropathics and steroid injection have little meaningful benefit for people with sciatica. But anyone with an ounce of common sense would know that this doesn’t mean these things “don’t work”, and anyone with half a heart would know this doesn’t mean we shouldn’t think about using them. So much of the decisionmaking in this space comes down to clinical experience, knowledge of the mechanisms, and your own philosophical stance on what research evidence *is*. (Which Raymond and I talk about in the podcast!)
* Book update! Here’s a photo the kanban for the book - this is just the first part, “What is Sciatica?” Sticky notes go from the “pending” column to “researching”, then “writing”, then “editing”, then (empty so far!), “done”. (If the photo looks confusing to your eye - the sticky notes are on a mirror!).
So far, I have written 30,000 words of this section. I expect it will get shorter (and better) as I edit and cut. To help me along I have made a contract with my mate Nils where he gets £1,000 from my account if it’s not finished by February 1st… Nils is exactly the kind of person who would happily take my money, so this is a good extra bit of motivation.
But today is Sunday so I’m off to play tennis! As a reward for Houston being near-uninhabitable in the summer, we are enjoying warm, sunny days in November.
Til next time,
Tom
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Thanks for reading the 17th edition of my sciatica newsletter. This newsletter tracks my research into all things lumbar radicular pain!
For this week’s podcast I spoke to Mark Laslett! Here’s the timestamps for our conversation, with some links to one or two papers Mark mentions:
1:38: On somatic referred pain.
2:40: “Do you have a theory of what's going on when someone has radicular pain but their MRI does not show anything to explain it?”
7:11: “Does largely compressive radicular pain have a different clinical picture to largely chemical?”
12:10: The role of injections in the wider treatment plan. Mark refers to this study.
16:20: Using screening questionnaires.
19:25: Mark's approach to practice and different treatment modalities.
24:50: How treatment of radicular pain has changed over time, the natural time course of radicular pain and speed of onset as a predictor of recovery.
30:44: “Is there a role for exercise in treating someone whose radicular pain does not centralise?”
33:33: “Are there any long term restrictions on movement after radicular pain has settled? And for squatting and deadlifting specifically?” Mark refers to this paper.
39:39: The role of anti-neuropathic pain medications.
43:40: Coming changes to Mark's online course and treating low back pain when research and guidelines feel vague
Thanks to Mark for taking the time to talk. I sent him a list of questions ahead of time but it got lost in an email thread so he didn’t see it. When we realised this before recording, he said “Well if I needed to prepare to answer your questions, I shouldn’t be answering your questions!”. What a pro!
Other bits and bobs
* I was mortified to notice I’d commited a typo in the *title* of last week’s newsletter. But, no one noticed… right?
* Tina has updated her already-brilliant website Living Well With Pain so now it’s even better. Great, practical information for patients and clinicians on sciatica, in particular persistent sciatica.
* Here’s another really impressive spinal cord prosection
* A new RCT by Julie Fritz and colleagues randomized 220 people with sciatica to receive usual care or usual care with four additional sessions of physical therapy. After six months, the early physical therapy group had an average 5.4 points better score on the Oswestry and an average 1 point less back pain - differences of debateable clinical importance. There was no average difference in leg pain.
Unfortunately, I cannot access the full paper yet so I don’t know what the PT consisted of, or what they classed as sciatica etc. But the results seem disappointing although not that surprising. I think it’s really valuable to get an idea of how much PT treatment affects radicular pain so that we can decide how best to spend our time with patients and advise them on what to expect.
Incidentally, the paper seems to be a very similar design to an older paper by Luijsterburg et al., and both found that patients getting extra PT reported greater treatment success but that their symptoms weren’t that different.
* Here’s my chat with Jack Chew, talking about research (maybe not much new to readers of this newsletter) and from 18 minutes on I pretend I have it all figured out when it comes to social media and news consumption.
Til next time!
Tom
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Thanks for reading the 15th edition of my sciatica newsletter. This newsletter tracks my research into all things lumbar radicular pain!
Today I was up bright and early to attend Annina Schmid's online course on assessment of entrapment neuropathies. Annina was kind enough to talk with me afterwards for a podcast! Our conversation mostly focused on the mechanisms underlying radicular pain.
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
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.
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
Other bits and bobs
* I recommend this Words Matter podcast with Rani Lill Anjum.
* These diffusion tensor imaging pictures of lumbar nerve roots are beautiful! From Shi et al. and Eguchi et al.
That's it for this week! I'm off to bed now to wake up early again (on US time) for Colette Ridehalgh's half of the course tomorrow, on treatment of entrapment neuropathies.
Til next time,
Tom
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Thanks for reading the 13th edition of my sciatica newsletter. This newsletter tracks my research into all things lumbar radicular pain!
This week I’m talking to Giacomo Carta.
Giacomo is a basic science researcher in neuromechanics, neurorepair and neuroplasticity. He’s also a physical therapist! We discussed his research and his hopes for the future of neurodynamics, nerve pain treatment and physiotherapy in general.
I hope you enjoy our conversation.
Tom
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Thanks for reading the 11th edition of my sciatica newsletter. This newsletter tracks my research into all things lumbar radicular pain!
This week's podcast is a Sciatica Story with Drew Jordan
Drew got sciatica about one year ago. He was on holiday and tried surfing for the first time which seems to have triggered it, and he spent a lot of time sitting which seemed to make it worse.
After one or two false starts and misdiagnoses, he found out what was causing the pain, found a physical therapist who helped him a lot, and started making progress with his pain. He recently made a video on youtube explaining his approach and what worked for him called Sciatica Survival Guide.
Drew has an incredible systematic, reflective, “big picture” approach to getting on top of his pain.
His video, and I hope this podcast, will be helpful to clinicians and people with pain alike. I think it will be particularly useful for anyone who is trying to work out their personal “pain triggers” and how to manage them.
I hope you enjoy our conversation!
Tom
Links:⚡ Drew’s Sciatica Survival Guide
⚡ Drew’s Sciatica Playlist
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This is a repost from 2018, an article caled Wired Into Pain: a history of the science of pain. I hope you enjoy it. I’ve also recorded an audio version to go with it!
[2024 AUTHOR’S NOTE: I think this piece (from 2018) is still a hugely valuable introduction to the history of pain science, rich in detail. But there are some mis-steps towards the end, where it veers into a bit of a triumphalist view of recent pain science. I can’t spot much that is flat-out wrong, but I wish there were other perspectives. Don’t let that put you off reading].
I am a Physiotherapist. Almost every person I see in clinic is in pain, and most already have an idea about what has caused their pain. If they are old enough, they might say ‘overuse’, or ‘wear and tear’; if they are younger, they might say ‘bad posture’ or ‘tight muscles’; if they have had a scan, they might say a ‘slipped disc’ or a ‘bone spur’. We accept these explanations prima facie. We consider pain to be a readout on the state of the body’s tissues. Or, as one doctor wrote in 1917, it is “the unerring medical compass that serves as a guide to the pathological lesion”.
But it is only very recently that we have come to understand our aches and pains in this way. Since medieval times, until surprisingly recently, people commonly understood their pains in terms of their relationship to God, often as punishment for sin. Physical and emotional pain were entangled, along with mind, body and soul. This was the grim logic of medieval torture and self-flagellation: the truth of the soul could be accessed through the pain of the body.
But, as historian Joanna Bourke records in her book The Story of Pain, this mixture of mind, body, soul and God also allowed people to feel pain as comforting: a “vigilant sentinel […] stationed in the frail body by Providence”, as one writer put it in 1832. For others, pain was redemptive: take, for example, the early nineteenth-century labourer Joseph Townend, who resolved himself to God after undergoing surgery without anaesthetic, and reflected at the end of his life on his “sincere thanks to the Almighty God” for his agonising conversion.
Pre-modern physicians had a different perspective. Most understood pain according to humoural theory. Hippocrates and his disciple Galen considered all illness to be caused by an imbalance of the body’s humours — phlegm, yellow bile, black bile and blood — which ebb and flow in response changes in the body or its environment. This notion endured for many centuries. To one 18th century writer, pain was a consequence of “viscid blood [stopping] at every narrow passage in its progress”; to another, it was a “Nature throw[ing] a Mischief” about his body. Humoural theory is pre-scientific and seems quaint to us now. But, as Bourke points out, it accounts for an abundance of influences, from our personal temperament and our relationships to the alignment of the planets above our heads, on the pain that we feel.
Over the coming centuries, at great cost to people suffering from pain, this insight was lost. This is the story of that loss; of how we arrived at the strange, wrong idea that pain is a straightforward “guide to the pathological lesion”; and of how an emerging re-understanding of pain shows us that it is more complex and more astonishing than we have thought for centuries.
Descartes, dualism and the labelled line
“The ghost in the machine” — Gilbert Ryle
It is in the sixteenth century that we find the beginnings of the dominant modern understanding of the body and its pains. The rise of Protestantism and, amongst secular thinkers, of humanism, contributed to an increased focus on the individual and an understanding of the body as a natural, rather than a supernatural entity. Medicine became more interested in anatomy and the physical laws of nature. Vesalius published his On the Fabric of the Human Body, a compendium of illustrations of dissected cadavers based on the author’s strict, first-hand observations at a time when doctors were not accustomed to performing their own dissections. Later, physicians like William Harvey took principles from physics and astronomy to show that in many ways, our bodies can be understood as machines: pumps, pulleys and levers. Slowly, the body became less sacred and more scientific.
It was in this spirit that, in 1641, the French polymath Renes Descartes published his Meditations on First Philosophy. This work contains a drawing that became the seminal image of pain for the next three hundred years. The picture shows a kneeling boy with one foot perilously close to a small campfire. The heat of the flame sends a signal (an “animal spirit”) up a channel to the boy’s pituitary gland, which Descartes reckoned was the seat of consciousness. There, the signal elicits pain, “just as pulling one end of a cord rings the bell at the other end”.
This picture makes sense to us, it seems intuitively correct. But this is because in matters of pain we are most of us now, in the Western world at least, the children of Descartes. For pain scientists on the other hand, who have fought in recent decades to emancipate themselves from Descartes, this picture has has come to represent the original sin, the first big lie of the Western world’s understanding of pain.
It’s crimes are twofold. First, it is the essence of an idea called dualism, which holds that mind and body are separate. The body feels pain, and passes this information on to the mind. For Cartesian dualists, the body is a machine and we are a kind of ghost in the machine, receiving information about its status.
Second, the picture represents pain as being felt by a specific detector in the body, and passed up a specific pathway, the long hollow tube, to a specific location in the boy’s brain. Pain detectors, at the end of a pain pathway, that leads to a pain centre. This idea is called specificity theory, but in this post I’m going to use the term labelled line theory because although it is less common, I think it is more descriptive — a labelled line for pain.
As it happens, Descartes’ idea was more subtle than the picture and its subsequent interpretations made out. In his defence, the historians Jan Frans van Dijkhuizen and Karl A.E. Enenkel point out that Descartes knew that pain is not merely perceived, like a mariner perceives his ship, but felt, as if the mind and body are “nighly conjoin’d […] so that I and it make up one thing”. Descartes knew that we don’t just have a body; we are a body. But this subtlety was lost: the picture of the little boy with his foot in the fire has a memetic power that has carried it, along with dualism and the labelled line, through the centuries.
The nineteenth century
“Nothing less than the social transformation of Western medicine” — Daniel Goldberg
This change came gradually. It was not until the nineteenth century, two hundred years after Descartes’ Meditations, that dualism and the labelled line for pain finally established their authority in medicine.
They set in as part of a wider change in the history of medicine following the French Revolution that is sometimes now called the ‘Paris School’. The physicians of the Paris School transformed large teaching hospitals in the city to dedicate them, for the first time, to furthering scientific knowledge through rigorous observation of patients and cadavers, and the classification of disease. They explicitly rejected humoural theory, which held that illnesses are processes that are distributed around the body through the movement of viscous humours. Rather, physicians of the Paris School considered diseases to be the result of lesions localised to a single, solid organ.
Influenced by the Paris School, Victorian physicians across the Western world began to search their suffering patients’ bodies for a local, solid lesion to blame for their pain. As one New York physician wrote in 1880, “we fully agree that there can be no morbid manifestations without a change in the material structure of the organs involved”. For the first time, doctors began to think like detectives on the hunt for the smoking gun, following clues provided by the body and its sensations (it is no coincidence that Arthur Conan Doyle was a doctor before he wrote the Sherlock Holmes stories, or that he made his character Watson one, too).
This approach has tremendous diagnostic power. But, as we will see, even modern researchers find that our pain, particularly our chronic pain, resists reduction by detective work. How did Victorian physicians respond when their investigations failed to turn up a local lesion to explain pain? According to historian and medical ethicist Daniel Goldberg, many doubled down, hunting for anything they could find. As one surgeon put it, “any lesion anywhere in the body will do to account for an otherwise inexplicable pain”. And that meant any lesion: the surgeon Joseph Swann, or example, baffled by a woman’s 11-year history of pain in an apparently healthy knee, eventually attributed it to an imperfection he found, after much searching, in a nerve in her hand.
Those that could not find a lesion anywhere explained unexplained pain as one inevitably must if one subscribes to the logic of dualism: if it’s not in the body, it must be in the mind. Goldberg tells the story of the surgeon Josiah Nott who, in 1872, took on the care of an American soldier whose leg was crushed in a railway accident. The leg had already been amputated by another surgeon at a point about halfway up the calf, but the soldier had developed phantom limb pains. The original surgeon, assuming there must be a local lesion at the end of a labelled line, had then amputated the stump, but to no avail. Nott, making the same assumption, took still more from the stump the next year, and still the patient felt no relief. Later that year, Dr. Nott operated again, removing tissues from three major nerves in the shank. This pattern continued until Nott had removed the poor soldier’s leg up to four inches above the knee, and his sciatic nerve up to the pelvis. When the patient’s pain returned after this final operation, Dr. Nott reasoned that he must have acquired an addiction to opioids which was inciting him to malinger (to exaggerate or feign his disease). Nott had, horribly literally, followed the assumed cause of the disease up a labelled line through the body and, not catching it, decided it must therefore be in the mind.
This logic played out on a broad scale in physicians’ understanding of the now-forgotten condition “railway spine”, the widespread and mysterious back pain felt by the victims of train accidents. Initially, physicians thought that the trauma of a crash caused compression of nerve filaments that in turn caused pain. But as time wore on and their investigations repeatedly failed to find a tissue lesion to explain railway spine, even in cadavers, their suspicion grew that railway spine was not a ‘real’ condition at all. After all, weren’t most victims also seeking compensation from railway companies? By the beginning of the twentieth century, railway spine was known instead as “hysterical spine […] merely a psychical condition”. Dualism dictated once more that if we can’t find it in the body, it must be in the mind.
1900 to 1965
Anomalies, non-anomalies, and opening the gate
Anomalies
“[Pain] reveals only a minute proportion of illnesses and often, when it is one of their accompaniments, is misleading. On the other hand, in certain chronic cases it seems to be the entire disorder which, without it, would not exist.” — Rene Leriche, 1937
The break from Cartesianism began at the end of the nineteenth century, when the great neuroscientist Santiago Ramon y Cajal showed that our nerves, spinal cord and brain are not one thing but composed of many smaller things (which came to be called neurons) linked by gap junctions (which came to be called synapses). Decades earlier, the English neuroscientist Charles Bell had suggested that the function of the nervous system is less straightforward than the labelled line in Descartes’s picture, and Cajal’s work was proof.
As we can see by his extraordinary drawings, Cajal meticulously mapped the peripheral neurons in our arms and legs, running to the spinal cord, and the neurons running up the cord, and many of those in our brain. But, according to pain scientist and writer Fernando Cervero, the terminus for incoming peripheral neurons, the foremost part of the spinal cord that we now call the dorsal horn, was so dense and chaotic that it resisted even Cajal’s fastidious eye. He called the dorsal horn a maremagnum, a Spanish word that means ‘confused and disorganised crowd’, as in the bustle of a busy railway station. Cajal’s vision of a network of individual cells, with nodes of incomprehensible complexity, opened up the possibility that signals aren’t simply passed upwards in a linear fashion as Descartes had assumed, but are modulated along the way.
The idea that inputs to the nervous system are modulated before they ‘become’ our sensations hints at an explanation for the odd persistent pains for which Victorian physicians could find no lesion. It also begins to explain the opposite phenomenon, lesions that cause no pain, which became unignorable during the brutal first decades of the twentieth century. Doctors like Rene Leriche, on the front line in the Great War, found that soldiers with dreadful wounds often felt no pain and could undergo surgery without anaesthetic. Leriche knew this was not willpower but “certain movements of the hormones, or of the blood”, a presciently non-Cartesian thought.
During the Second World War, the American anaesthesiologist Henry Beecher built on Leriche’s observations by conducting a more methodical study at his post in Italy. He found that as many as three quarters of wounded soldiers felt little pain at the time of their injury. As one doctor put it, it was as if wounds and diseases “carry for the most part — most mercifully — their own anaesthetics with them”.
One might think that such cases would have alerted the scientific community to the fact that our nervous systems are doing something more than passively relaying pain into our brains, as labelled line theory implied. But for scientists and doctors at large, anomalies that defied labelled line went on hiding in plain sight, “discovered” periodically and then easily forgotten as they had been in the Victorian era. Phantom limb pain, for example, was unignorable during the American Civil War, and then slipped once more from popular consciousness. The doctor and writer Oliver Sacks called these periods of forgetting scotoma, dark gaps in the scientific awareness in which the prevailing theory cannot explain common phenomena and instead shoves them in the attic to think about another day. The progress of science, wrote Sacks, is faltering and haphazard, “very far from a majestic unfolding”.
Non-anomalies
“Pain is the physiological adjunct of a protective reflex” — Charles Sherrington, writing in 1900
“Pain remains a biological enigma — so much of it is useless, a mere curse” — Charles Sherrington, writing forty years later.
(Quoted in Understanding Pain by Fernando Cervero)
Rather than explaining anomalies, scientists studying pain at the beginning of the twentieth century focused on a series of discoveries that appeared, at first, to confirm labelled line theory. The British neuroscientist Charles Sherrington had coined the term “nociceptor” for the neurons that convey danger messages (elicited by things like heat, intense mechanical pressure or an incision to the skin) to the brain, and in the following decades researchers slowly but successfully identified and isolated these cells.
Starting in 1912, American scientists performed the first anterolateral cordotomy, slicing through the part of the spinal cord that was theorized to carry danger messages to the brain and appearing to stop pain in its tracks. Later, the success of such operations would prove to be temporary, but the procedure did show that this part of the spinal cord houses Sherrington’s nociceptors. In 1927, the Americans Herbert Gasser and Joseph Erlanger established that different nerve fibers conduct signals at different velocities, and classified them according to their diameter as A, B and C fibers. A fibers were widest and conducted signals the quickest; C fibers were the most narrow and slow. They found that one sub-type of A fibers, A-delta fibers, conducted the relatively quick sensation of dull pain we feel when we stub our toe; and that C fibers conduct the slower, stinging pain that arrives later. Again, this neat distinction would later prove to be more complicated, but the discovery was further evidence for a labelled line of pain. Gasser and Erlanger were only able to look at conduction signals from a whole bundle of nerves and so it was not until 1958 that Ainsley Iggo was first to record individual A-delta and C fibers and isolate Sherrington’s nociceptors for the first time.
Opening the gate
“It may seem easy, but it was not” — Ronald Melzack
Despite this series of discoveries in favour of labelled line, some researchers could not shake from their minds those confounding anomalies: pain without lesion, and lesion without pain. And so, at last, the science of pain began to wake from its scotoma. Some scientists began to propose a theory to compete with labelled line called pattern theory, which held that it is not the stimulation of specific nerves that causes the sensation of pain, but that the way in which nerves are stimulated, spatially and temporally. Pattern theory was vague, and had nowhere near the amount of evidence that supported labelled line theory, but it did hint at an answer to some of the anomalies that had been documented in the recent scientific literature, such as the way pain spreads beyond the site of an injury and the way rubbing a pain can make it temporarily feel better. Pattern theory was taken up in Oxford in the 1940s and 50s, where the brilliant British neuroscientist Pat Wall was beginning to develop ideas he would turn into gate control theory, a whole new model of pain.
In 1959, Wall moved from Oxford to the Massachusetts Institute of Technology where he met Ronald Melzack. Melzack, a Canadian, had just arrived at M.I.T. to take up a post as assistant professor of Psychology, and found to his annoyance that he could not perform research on animals in the university’s Psychology building. So, Melzack decamped to Wall’s lab. The two quickly took up a discussion on the inadequacy of Cartesianism and decided to come up with a new theory to “entice spinal-cord physiologists away from [labelled line]”.
From his previous research, Melzack knew the brain sends messages down the spinal cord to inhibit the messages coming up it, exerting a kind of ‘top-down’ control on incoming information. From his own experiments, inspired by pattern theory, Wall knew that different inputs into the nervous system are weighed against each other somehow in the spinal cord, competing to be ‘sent up’ to the brain. Despite their discussions, Melzack and Wall’s ideas remained inchoate until, in 1962, Melzack stumbled on the Dutchman Willem Noordenbos’s pattern-theory hypothesis that large A-fibers carrying touch signals might somehow inhibit small C-fibers carrying danger signals.
Melzack calls this moment a “flash of insight”. Noordenbos had theorized that this modulation happened in the substantia gelatinosa, which is part of the terminus for incoming information at the spinal cord. Wall knew that large fibers and small fibers entered the substantia gelatinosa at opposite ends, and theorised that it was this setup that allowed the one to inhibit the other, like closing a figurative ‘gate’. The weight of signals from large and small fibers would determine what kind of message was allowed up to the brain.
In 1963, Melzack moved to McGill University in Canada, but travelled South over the border when he could to visit Wall’s home in Boston where, over large amounts of duty free whiskey, the two put the finishing, definitive touches to their work. Their theory differed critically from Noordenbos’ because they proposed that the brain itself plays a role in processing at the substantia gelatinosa, by sending signals down the spinal cord to make the ‘gate’ more likely to open or close to danger signals. This was gate control theory.
For the first time, science had a model that began to explain pain anomalies. According to gate control theory, for example, the brain of a soldier who has sustained an injury can send messages down the spinal cord to close the gate to incoming danger signals. Over fifty years have passed, and gate control theory has turned out to be wrong in lots of little ways, but right in one big way: it is modulation in the spinal cord and the brain, or the central nervous system, that explains why pain is so rarely the reliable sign of tissue status that Victorian scientists assumed it was.
Neuromatrix theory
“We need to go… to the brain” — Ronald Melzack
“When you feel a pain in the leg that has been amputated, where is the pain? If you say it is in your head, would it be in your head if your leg had not been amputated? If you say yes, then what reason have you for ever thinking you have a leg?” — Bertrand Russell
Gate control theory was a great advance but Melzack and Wall knew their theory was incomplete. According to Oliver Sacks, it is by studying anomalies — phenomena not explained by the prevailing theory — that researchers wake from scotoma and begin revolutions in scientific understanding. So it was that Melzack’s interest in the anomaly of phantom limb pain led to neuromatrix theory, the next great boost that finally allowed pain science to escape to orbit of Cartesianism
If people without limbs have phantom pain, Melzack reasoned, it follows that the origins of the pattern of pain lie not in the limb but in the brain. And not only pain, but the sensation of having a body in its entirety — its place in the world, its shape, its movements — is housed, in what Melzack came to understand as a series of loops and patterns of neurons, inside our brains. This brain architecture is the neuromatrix.
Incoming information, then, is not what holds the essence of our sensations; it merely triggers the neuromatrix, already inscribed in the brain, to ‘produce’ the sensations we feel. If a boy puts his foot in a fire, the nerves do not tell a passive brain “here is pain”; the nerves simply say “here is an intense input”, and the neuromatrix does the rest.
How do we get a neuromatrix? Melzack says it is inborn, but then shaped by experiences. So, your neuromatrix develops your own personal signatures for familiar pains, like the pain you might feel in your back when you bend. Crucially, the neuromatrix uses our thoughts and emotions to generate our sensations, as well as sensory information. This makes sense: think of a stroke on the leg from your partner and one from an unappealing stranger. The same sensory input feels different.
So, if you believe the cause of your back pain is something threatening, like a suspected spinal cancer or a ‘slipped’ disc, it willfeelworse than if you believe it is something benign, like a muscle strain. If a conscripted soldier sustains a battlefield injury that means he will likely have to leave the trenches to convalesce behind the front lines, that wound may not feel as bad as it would for a factory worker, for whom it could mean a loss of livelihood. If you have just been made redundant, or become divorced, than the incoming danger signals from an incipiently arthritic hip might suddenly start triggering your neuromatrix to produce a deep aching pain in your joints.
Pain is intimately integrated with meaning, and informed by the broader context of our lives. And there is no labelled line: pain is the output of a widely-distributed neural process that takes input from countless biological, psychological and social factors.
The sensitive nervous system
“Not under conditions of my choosing / Wired into pain / Rider on the slow train” — Adrienne Rich
Researchers have used the neuromatrix as a foundation to develop our understanding of pain. For example, towards the end of the 1970s, scientists began to establish that the endings of our danger messenger neurons, the ones Sherrington christened nociceptors, become more sensitive the more they are used, a process called peripheral sensitization. But perhaps the most remarkable development since Melzack proposed the neuromatrix was Clifford Woolf’s discovery of central sensitization.
On completing his medical training in South Africa in the early 1980s, Clifford Woolf joined Pat Wall’s laboratory in London. He was not content with measuring the readouts from individual chains of neurons, and instead began to monitor broader bursts of activity which he thought would give him more insight into the pain system as a whole. He started to measure the output of the neurons that cause muscles to flex away from a dangerous stimulus (think of touching a hot stove and retracting your hand before you are even conscious of pain). Investigating on rats, he found that most of these cells responded to dangerous stimuli, such as heat and pinch, in a fairly narrow field — say, one toe. But, some cells had a very wide receptive field and would respond to even light, non-dangerous touch. Why would rats have neurons designed to elicit a withdrawal response to light touch?
It took Woolf some months to realise that he was only finding these neurons at the end of the workday, when his rats had already been subjected to hours of pain-inducing stimuli. He calls this his “eureka moment”. He had not discovered that rats have certain neurons that are super sensitive across a wide receptive field: he had discovered that a rat’s nervous system becomes super sensitive across a wide receptive field when it has been exposed to prolonged danger. Woolf had discovered an ‘amplifier’ mechanism in the spinal cord. This phenomenon is central sensitization.
Woolf was the first person to show that the nervous system is not hard-wired for pain but plastic. Prolonged nociception can change the behaviour and the architecture of the nervous system so that non-dangerous inputs (like light touch) are felt as painful, and dangerous inputs (like a pinprick) produce more pain than they otherwise would have done. To top it off, this whole pain experience also spreads beyond the original site of injury. The great physiotherapist Louis Gifford described central sensitization as like tapping X on your computer keyboard three times, and 10 X’s of different sizes and colours popping up on the screen.
A mild and benign form of central sensitization is common and almost immediate after most injuries — after you burn your hand or sprain your ankle, it is your body’s way of protecting itself. But central sensitization can wear on and, in many cases, persist and get worse long after any injury has healed. If you or someone you know has widespread back pain that flares up with the slightest movement, or has osteoarthritis in their hip that seems to spread all the way down their leg, they might have central sensitization.
Central sensitization can affect many different functions, not just pain. People with ongoing, maladaptive central sensitization can be tense and forgetful, and sensitive to bright lights, loud noises and chemicals. It is also a feature of irritable bowel syndrome, migraine and chronic fatigue syndrome, and often goes hand in hand with anxiety and depression.
So long, labelled line: Grappling with complexity
“Pain cannot easily be divided from the emotions surrounding it. Apprehension sharpens it, hopelessness intensifies it, loneliness protracts it by making hours seem like days. The worst pain is unexplained pain” — Hilary Mantel
“The basic idea of pain modulation implies that the output can be different to the input at every stage in the transmission of pain signals throughout the brain” — Fernando Cervero
Central sensitization is just one discovery that has enhanced our understanding of pain. There are many more examples. Descending modulation is the ongoing process by which the brain sends signals down the spinal cord to simultaneously inhibit and facilitate incoming danger signals, a mechanism Leriche anticipated when he observed that battlefield wounds “carry […] their own anaesthetics with them”. In people with persistent pain, descending modulation may be set for a net facilitation of incoming danger messages. Researchers have also expanded our understanding to include the immune system, which aids and abets the nervous system as it produces pain. They have found out that nociceptors, far from lying waiting for an intense stimulus as Sherrington imagined, are actually firing regularly throughout the day, every time we use a pair of scissors, ride a bike or go on a long walk, without (if we are lucky) our neuromatrix producing the experience of pain. Conversely, clever experiments have shown that nociception is not even necessary for pain, giving credence to the stories of people who narrowly escape injury but, believing they have been hurt, writhe in agony. And, we know that stress, even the stress of early life events, plays a vital role in ongoing pain, and that our stress system and pain production system are intimately linked.
The contrast between the byzantine, distributed complexity of the mechanisms of pain and the singular experience of pain — I feel it here — is remarkable. Scientists have made various attempts to simplify the mechanisms into something more understandable and more useful to lay people. The neuroscientist VS Ramachandran has said that “pain is an opinion on the organism’s state of health rather than a mere reflective response to an injury”, a stark contrast to the old-fashioned idea of pain as “the unerring medical compass that serves as a guide to the pathological lesion”.
The scientists and physiotherapists Dave Butler and Lorimer Moseley put it elegantly:
“We will experience pain when our credible evidence of danger related to our body is greater than our credible evidence of safety related to our body. Equally we won’t have pain when our credible evidence of safety is greater than our credible evidence of danger.”
In other words, pain is not measuring damage, it is a protective strategy, just one of many (along with local and systemic inflammation, changes in movement like tensing or bracing, the feeling of stiffness, and so on) that the body enacts in response to credible evidence of danger.
This evidence of danger often includes nociception (signals from tissue damage), but the neuromatrix uses many other sources, too. For example, if someone has back pain and a doctor tells you your x-ray shows “wear and tear” or “degeneration” in your spine, they have received a clear message of danger related to your body that is likely to make their pain worse. Indeed, people with back pain who get an MRI actually reduce their chances of recovery. On the other hand, if that person’s doctor (or physiotherapist!) tells them that the findings on their scan are normal age-related changes (or, better yet, doesn’t order a scan at all), that is a clear safety message. Safety messages can come from anywhere. Exercise can send safety messages to your neuromatrix, and so can a supportive workplace or having a friend around to talk to.
Reflections
Slow progress, hopes for the future and a note of caution
Slow progress
“I am still not happy with what has been accepted” — Pat Wall, 1999
Danger sharpens pain; safety soothes it. Why, then, do health professionals continue to give people with persistent pain credible evidence of danger? Apart from the obvious — that there is money in telling people their spines are crumbling and their pelvises are out of line, that they have muscle knots that need releasing and cores that need stabilizing — it is because, just as Descartes’ model of pain took almost three centuries to reach its zenith in Western culture, the neuromatrix, still only forty years old, has been accepted only falteringly even in medical circles, and hardly at all in the wider culture.
Indeed, in many ways the twentieth century has doubled down on labelled line. Take, for example, the dominance of the orthopaedic understanding of low back pain, which the late Scottish doctor and historian Gordon Waddell called “the dynasty of the disc”. Waddell traces the tenuous association of the lumbar disc with low back pain to a fateful cluster of papers published at the beginning of the century by orthopods searching, like Victorian physicians had done before them, for a pot of gold at the (wrong) end of the labelled line. Even today, routine orthopaedic surgeries like lumbar fusion, knee arthroscopy and shoulder decompression are amongst the most low-value, least evidence-based treatments in healthcare, still performed largely because of inertia and unexamined Cartesianism.
Many physiotherapists practice with the same habits. Like Joseph Swann, we might conduct a questionable root-cause analysis up or down a kinetic chain to find an ‘issue in the tissues’, settling on a pronated foot, a slumped posture or a valgus (in-falling) knee. Like Josiah Nott, when a patient has failed a course of ‘corrective’ exercise to ‘fix’ their body we might decide their problem is primarily ‘psycho-social’, a euphemism for in-their-mind. This is understandable, it takes great effort to shift from Cartesianism to the neuromatrix; I have been trying for years and I am still astonished when a new study is published showing, for example, that there are no major physical risk factors for a first episode of neck pain, but multiple psychological ones, like depression, and social ones, like role conflict. Still, it is imperative that medical professionals of all stripes challenge their colleagues who promote themselves as experts but who practice with unreconstructed Cartesianism.
Hopes for the Future
“While pain sufferers do not have the luxury of denying the reality of their pain, they can and do deny its legitimacy, thereby internalising the stigma so frequently directed at people in pain.” — Daniel Goldberg
The neuromatrix model has the potential to be immensely liberating for patients. For people with everyday predicaments of life like the back or shoulder pain we all get from time to time, there is the reassuring message that pain is not an indicator of damage and they are safe to move. In fact, movement, as opposed to protecting the painful joint, is the way to go in the long run. For people with more profound, widespread and recalcitrant pain, understanding why their pain is the way it is can help with the process of acceptance, and knowing pain is multifactorial can open up new therapeutic options to help calm down a sensitive nervous system.
The neuromatrix could also militate against the way Cartesian thinking drives stigmatization of people with chronic pain. Cartesian dualism casts pain as a two-step sequence of events: the body senses pain, then the mind reacts. As recently as the 1980s, words like “hysterical” or “psychogenic” were used to describe people who appeared to be ‘over-reacting’ to their pain. It is this thinking that allows us to sort people into those who are responding appropriately to their pain, and those who are ‘being dramatic’. The saddest effect of this stigma is when patients internalise it, believing that they are not ‘coping’ properly with ‘a bit of back pain’.
So patients and health professionals need to know that dualism is bogus: as Pat Wall himself put it, “the separation of sensation from perception was quite artificial… sensory and cognitive mechanisms operate as a whole”. Or, in the words of neuroscientist Fernando Cervero, “emotional, sensory and cognitive elements aren’t organised in a hierarchical way, but in a cooperative way […] interacting to generate the final pain experience”.
A note of caution
“Nineteenth century physicians drain[ed] pain of any intrinsic meaning altogether, making it little more than a sign or symptom of something else” — Joanna Burke
“[The challenge is] to allow a rapprochement between the world of the clinician and the world of the person in pain” — Quinter et. al (2008).
The neuromatrix and all its attendant discoveries have revolutionised how medical and health professionals should approach people in pain. It is a rare true paradigm shift. But there is danger in complacency. “Now is not a time for professional hubris or the proclamation of truth by a few”, warn the rheumatologists John Quintner and Milton Cohen. The battle to understand pain is only half won. It is all too easy to be drawn back into the orbit of dualism, not only between the mind and body, but between the clinician and the patient, or the researcher and the sufferer. Centuries-old habits die hard, and we have long made the person-in-pain an object of enquiry. But this can only take us so far; as Quinter and Cohen assert, “the pain of another person is irreducible to its neuronal correlates”. We can only really know pain through dialogue.
It is difficult to talk properly about pain. Being in deep pain can be a harrowing, abject, solitary experience. And apart from anything else, often we just don’t have the words: Virginia Woolf, no stranger to pain, lamented that English has a rich vocabulary for love, but a meagre one for pain. The poet Emily Dickinson said that pain “has an element of blank”.
But it can be done. Joletta Belton, a blogger with persistent pain, recently tweeted about the two clinicians who had helped her the most. “It wasn’t just their words” she wrote, “it was that they listened first. And understood. Listening matters […] I wasn’t interrupted or lectured, they didn’t try to ‘educate’ me or alter my narrative to suit their own […] I felt what I said was of value. I felt human, of worth. That’s invaluable.”
It may seem strange to end a post about science with a note on the importance of listening, but in the context of the neuromatrix it makes perfect sense. Listening to people in pain is what’s needed to undo the damage that has been done, and take the progress that’s been made to the next level.
Belton’s experience echoes a vignette reported by Joanna Bourke in The Story of Pain.During a medical consultation in 1730, an embarrassed patient found himself apologising to his physician for boring him with “so tedious a Tale”. The patient’s physician protested: “Your Story is so diverting, that I take abundance of delight in it, and your Ingenious way of telling it, gives me a greater insight into your distemper, than you imagine. Wherefore, let me beg of you to go on, Sir: I am all attention, and shall not interrupt you.”
Selected bibliography
Journal Articles
Allan, D. and Waddell, G. (1989). An historical perspective on low back pain and disability. Acta Orthopaedica Scandinavica, 60(sup234), pp.1–23.
Arnaudo, E. (2017). Pain and dualism: Which dualism?. Journal of Evaluation in Clinical Practice, 23(5), pp.1081–1086.
Baliki, M. and Apkarian, A. (2015). Nociception, pain, negative moods, and behavior selection. Neuron, 87(3), pp.474–491.
Bourke, J. (2014). Pain sensitivity: an unnatural history from 1800 to 1965. Journal of Medical Humanities, 35(3), pp.301–319.
Brodal, P. (2017). A neurobiologist’s attempt to understand persistent pain. Scandinavian Journal of Pain, 15(1).
Cohen, M., Quintner, J., Buchanan, D., Nielsen, M. and Guy, L. (2011). Stigmatization of Patients with Chronic Pain: The Extinction of Empathy. Pain Medicine, 12(11), pp.1637–1643.
Chapman, C., Tuckett, R. and Song, C. (2008). Pain and stress in a systems perspective: reciprocal neural, endocrine, and immune interactions. The Journal of Pain, 9(2), pp.122–145.
Eriksen, T., Kerry, R., Mumford, S., Lie, S. and Anjum, R. (2013). At the borders of medical reasoning: aetiological and ontological challenges of medically unexplained symptoms. Philosophy, Ethics, and Humanities in Medicine, 8(1), p.11.
Goldberg, D. (2012). Pain without lesion: debate among American neurologists, 1850–1900. 19: Interdisciplinary Studies in the Long Nineteenth Century, 0(15).
Goldberg, D. (2017). Pain, objectivity and history: understanding pain stigma. Medical Humanities, 43(4), pp.238–243.
Iannetti, G. and Mouraux, A. (2010). From the neuromatrix to the pain matrix (and back). Experimental Brain Research, 205(1), pp.1–12.
Kerry, R., Maddocks, M. and Mumford, S. (2008). Philosophy of science and physiotherapy: An insight into practice. Physiotherapy Theory and Practice, 24(6), pp.397–407.
Latremoliere, A. and Woolf, C. (2009). Central sensitization: A generator of pain hypersensitivity by central neural plasticity. The Journal of Pain, 10(9), pp.895–926.
Melzack, R. (1999). From the gate to the neuromatrix. Pain, 82, pp.S121-S126.
Melzack, R. (2005). Evolution of the neuromatrix theory of Pain. The Prithvi Raj Lecture: Presented at the Third World Congress of World Institute of Pain, Barcelona 2004. Pain Practice, 5(2), pp.85–94.
Melzack, R. and Katz, J. (2012). Pain. Wiley Interdisciplinary Reviews: Cognitive Science, 4(1), pp.1–15.
Mendell, L. (2014). Constructing and deconstructing the gate theory of pain. Pain, 155(2), pp.210–216.
Moayedi, M. and Davis, K. (2013). Theories of pain: from specificity to gate control. Journal of Neurophysiology, 109(1), pp.5–12.
Moseley, G. and Butler, D. (2015). Fifteen years of explaining pain: the past, present, and future. The Journal of Pain, 16(9), pp.807–813.
Moseley, G. (2007). Reconceptualising pain according to modern pain science. Physical Therapy Reviews, 12(3), pp.169–178.
Neilson, S. (2015). Pain as metaphor: metaphor and medicine. Medical Humanities, 42(1), pp.3–10.
O’Sullivan, P., Caneiro, J., O’Keeffe, M. and O’Sullivan, K. (2016). Unraveling the complexity of low back pain. Journal of Orthopaedic & Sports Physical Therapy, 46(11), pp.932–937.
Perl, E. (2007). Ideas about pain, a historical view. Nature Reviews Neuroscience, 8(1), pp.71–80.
Quintner, J., Cohen, M., Buchanan, D., Katz, J. and Williamson, O. (2008). Pain Medicine and Its Models: Helping or Hindering?. Pain Medicine, 9(7), pp.824–834.
Thacker, M. and Moseley, G. (2012). First-person neuroscience and the understanding of pain. The Medical Journal of Australia, 196(6), pp.410–411.
Wiech, K. (2016). Deconstructing the sensation of pain: The influence of cognitive processes on pain perception. Science, 354(6312), pp.584–587.
Woolf, C. (2007). Central sensitization. Anesthesiology, 106(4), pp.864–867.
Books
Cervero, F. (2014). Understanding pain. Boston: Mit Press.
Butler, D. and Moseley, G. (2015). Explain pain. Adelaide: Noigroup Publications.
Bourke, J. (2014). The story of pain. Oxford: Oxford Univ. Press.
Moseley, G. and Butler, D. (2017). Explain pain supercharged. Adelaide: Noigroup Publications.
Blog posts
Pain is weird by Paul Ingraham
Pain really is in the mind, but not in the way you think by Lorimer Moseley
Central sensitization in chronic pain by Paul Ingraham
My own chronic pain story by Paul Ingraham
Easing musculoskeletal pain Information leaflet
Tell me your story by Joletta Belton
Podcasts and lectures
The Pain Revolution by Lorimer Moseley
Pain: past, present and future with Mick Thacker
Understanding Pain in 2025 by Mick Thacker
This is a public episode. If you would like to discuss this with other subscribers or get access to bonus episodes, visit tomjesson.substack.com -
Welcome to the eighth edition of my sciatica newsletter!
This week’s podcast
In this week’s podcast, I talk to Michelle Angus. Michelle is a consultant physiotherapist working for the Complex Spinal Team in the Emergency Village of a tertiary spinal referral centre at Salford Royal NHS Foundation Trust. In this podcast, she tells me about:
* Managing radicular pain in the ED
* Spinal injections
* Spinal surgery
* Medications for radicular pain
* And much more!
So long, gabapentinoids?
In the podcast, Michelle shares her clinical experience with prescribing gabapentinoids to people with acute radicular pain. Her impression is that while they do not work for everybody, some of her patients get meaningful relief. In last week's podcast, Kate told me that gabapentin helped her own radicular pain. When I asked on twitter, I heard (mostly) similar stories: "gabapentinoids are sometimes the only thing that allows my patients/allowed me to get any relief". At the time of writing, NICE guidelines for sciatica don’t make a specific recommendation on gabapentinoids; instead, they direct the reader to the general guidelines for prescribing for neuropathic pain, which approve them.
But, the draft version of the updated NICE guidelines for low back pain and sciatica (released some weeks after my conversation with Michelle) recommends against them. According to the draft update, there is no evidence to support their use for people with sciatica.
Where do we go from here?
Gabapentin was developed in the early 1970s. It was approved in 1993 for seizures and marketed for pain soon after. Pregabalin arrived on the scene about ten years later. In the last two decades, their use has increased dramatically. Much of this has been “off label”, and the drugs have nontrivial side effects, so this increase is a cause for concern.
(Graph taken from Montastruc et al.)
Together we can call gabapentin and pregabalin gabapentinoids or anti-epileptics. Sometimes the term "anti-neuropathics" is used to bundle the gabapentinoids with tricyclic antidepressants like amitriptyline.
The gabapentinoids were designed to work on GABA, an inhibitory neurotransmitter, which is where they get their name. It turns out they don't do this. Instead, it seems they primarily work on voltage gated calcium channels.
You will remember that when an action potential arrives at the axon terminal, voltage gated calcium channels open to let calcium into the neuron. The calcium causes this first neuron to release neurotransmitters into the synapse, which trigger another action potential in the second neuron. After a nerve injury, more voltage gated calcium channels are expressed on the end of the injured first neuron, so more neurotransmitter is released, so the second neuron becomes more excitable, which can increase pain.
These voltage gated calcium channels are made up of smaller sub-structures, one of which is the α2δ subunit. It's this subunit that the gabapentinoids act on. As far as I can tell, we don't know exactly how. One theory is that gabapentinoids stop the subunits from being transported to the axon terminal in the first place. With fewer α2δ subunits, one link is weakened in the chain of synaptic transmission. And so that second neuron is less excitable.
There is a good deal of evidence that gabapentinoids work fairly well for neuropathic pain. The problem is, we can’t say the same for sciatica. The draft update to the NICE guidelines refers to only three studies. One is small, lower quality and found gabapentinoids worked quite well. The other two are large, high-quality trials, and say gabapentinoids are no better than placebo.
On reading that these large, high quality studies found no benefit, my first question was: Did they select patients with *neuropathic* radicular pain? After all, radicular pain is a very mixed bag of nociceptive, inflammatory and 'nociplastic' mechanisms, to name just a few. But I would only expect gabapentin to be effective for the subgroup of people with neuropathic pain, meaning actually damaged, not just irritated, nerves. People with severe shooting pain, numbness, pins and needles, etc. If the trials jumbled up these people with all the other mechanisms of back and leg pain, then no wonder their results are negative.
Picture from Schmid, Fundaun and Tampin (2020)
At first glance, it seems like these studies did indeed jumble up the different pain mechanisms. In the trial by Mathieson et al., only a third of patients had likely neuropathic pain (as measured by questionnaire) and half had no loss of sensation (which indicates true nerve damage). And the other trial, by Baron et al., didn't give enough detail on the patients to say whether or not they had neuropathic pain, which implies they too were a mixed group.
But on closer inspection, both studies did account somewhat for mechanism-based prescribing. Mathieson et al. did a post-hoc analysis to see if patients with neuropathic pain benefited more. There was no evidence they did. And Baron et al. did try and target patients by giving them a mini pre-trial to see if they were "responders" to pregabalin before enrolling them in the main trial. In the main trial, this group of "responders" didn no better with pregabalin than placebo.
Besides, even if there is a subgroup of neuropathic-pain "responders" hidden in these two trials, for the trials to show a null result there would have to be an equal but opposite group of people who got worse taking the drugs!
Where does this leave us?
The way I see it, there are four positions:
1. "Gabapentinoids don't work for radicular pain". People are saying this more and more, and it is probably true in most cases. But, it has a ring of certainty that is not supported by the evidence. (This is a soap box of mine, but I think we need to stop being so cavalier in saying "X doesn't work for Y"; most clinical trials aren't able to tell us this).
2. "There is no research evidence to support the use of gabapentinoids for radicular pain, and good evidence to show they are not better than placebo when prescribed according to common practice. Although anecdotally they seem to work for some people, we have no way of knowing whom, so we shouldn't risk it". This seems reasonable to me, especially considering the harms of these drugs, which I have not covered in this newsletter. If we have no way of knowing whether and how often we are doing something right, how can we justify doing it? Better to just cut it out until we can figure out a better way (researchers are currently working on "sensory profiling" to target prescribing for anti-neuropathics).
3. "There is no research evidence to support gabapentinoids for radicular pain, and good evidence to show they are not better than placebo when prescribed to a heterogenous group. So, we should prescribe them sparingly and cautiously, and only in people who have severe neuropathic radicular pain". This seems reasonable to me too! We shouldn’t limit ourselves to research that is of limited pertinence to our clinical problem just because it's the only research that exists (as in the fable of the drunk who has lost his keys and looks under a lamp post because it's the only spot that's illuminated).
4. "Gabapentinoids work for radicular pain". It goes without saying, this statement unjustifiable.
How to choose between (2) and (3) is tough. Luckily, I don't prescribe, so I don't have to make these difficult decisions myself! But I do have to make decisions about whether to refer people to clinicians who do prescribe. At the moment (possible guideline change notwithstanding), I would refer for consideration of gabapentinoids rarely and only in the following conditions:
* Severe, acute, disabling radicular pain
* Neuropathic pain, preferably as measured by questionnaire (although these are not really well validated: a topic for another newsletter)
* No option of epidural steroid injection any time soon
* Either the clinician or the patient has a good relationship with the prescriber
* The patient is in a service where they will get continuity of care and support with tapering if needed
As ever, I’d be really keen to hear your views, particularly disagreements and corrections.
Other bits and bobs
* Who should I talk to for future episodes of the sciatica podcast? I have already had some good suggestions on twitter. As a reminder, I’d also like to talk to people who have experienced radicular pain or clinicians with interesting case studies.
* The transcript of my podcast with David Butler is now available. Honestly, this was a huge ball-ache to write up, so I will see how useful it is to people before doing another one.
* I think at the moment it’s a bit odd that the podcast and the newsletter arrive in the same email, so in the future I might put the podcast out midweek instead…
* There was no newsletter last week as I was in Big Sur, celebrating my birthday and enjoying the return of the NBA :)
Big Sur view
With my niece, baby Ellie.
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Hi and welcome to the seventh edition of my sciatica newsletter!
This week's conversation is with Kate Charlton, a physiotherapist and triathlete from Northumberland, England. Kate has had two nasty episodes of sciatica and in this podcast she tells me about what it was like, what did and didn't work for her, and how she graded her return to sport. Our conversation will be a good resource to give to any of your patients who have radicular pain and train and compete at a high level.
We talk about
* Graded return to activity and “poking the bear”
* Kate’s very positive experience with gabapentin and neural gliding exercises
* Having hope and breaking negative cycles
As I mentioned, Kate has had two episodes of sciatica, both pretty intense. In my experience, the recurrence of sciatica can leave some patients completely distraught. After the first episode dies down, the relief must be immense. I can only imagine how sickening it must be to feel those same symptoms again.
How likely is it that lumbar radicular pain will recur after subsiding? We don't have a huge amount of information. In 2012, Suri et al. tracked 97 patients with MRI-confirmed disc herniation who received conservative care only. 79 of those patients reported a full recovery (not bad!). But of the patients who recovered, 25% reported a recurrence of their symptoms.
A few years later, Suri et al. investigated this further with a retrospective analysis of a large, multicentre trial of conservative treatment. After one year, the risk of recurrence was 23% - strikingly close to the 25% the authors found in their previous study. But at two years, this number rose to 41%, and at three years 51%!
To me, these numbers are disappointingly high. But Suri et al. do write that they may be over-estimating slightly. For one thing, there is a "background rate" of symptom reporting even in a non-clinical population. If you ask a lot of people whether they had radiating leg pain recently, as many as 10% will say yes. And, the outcome measure the authors used is probably sensitive but not specific: that is, it gets false positives from people who had, say, hip OA. Finally, we don't know how intense these recurrences were; perhaps some were faint echoes of the first episode. So, I don't think it is pushing it to say the picture might not be as bad as '1/4 of people experience a recurrence, rising to 1/2 in three years'. Nevertheless, we should be counselling our patients that recurrence is possible. Hard as that might be when we are likely sharing their immense relief.
What causes that pain to come back? Not always another disc herniation. In a 1997 study, Vik et al. got in touch with 211 patients who had received an operation for their lumbar disc herniations some years prior, in '88 and '89. 23% of those patients had had another operation in the meantime. Here's the thing: back then, MRI was not a routine part of investigations for people with sciatica. Surgeons would do a CT scan or something called radigulography (sounds like a drunk person saying 'radiculopathy’), but these are not as accurate. So, surgeons didn't quite know what to expect when they opened a patient up. In this case, they found about half of those patients who went for reoperation for their recurring symptoms didn't have a disc herniation at all.
There are a lot of explanations for this! For example, epidural adhesions, lateral stenosis... Following on from last week's newsletter, I also wonder if neuroinflammation is part of the picture. In one study (in mice!), an injury to a nerve root caused pain that slowly subsided and resolved after about six weeks. After pain had subsided, a second, identical injury caused significantly *more* pain than the first. The authors reckon this might have been caused by the persistent glial activation and inflammatory mediators, which were still present in the spinal cord after pain had resolved... The fact that contralateral sensitivity increased too also suggests this 'priming' is centrally mediated. Maybe lingering neuroinflammatory changes leave some people pre-sensitized to future stressors... (In this week’s podcast, Kate tells a great anecdote about an unusual stressor that reliably made her nerve root pain flare up.)
Other bits and bobs…
* Entrapment neuropathies: a contemporary approach to pathophysiology, clinical assessment, and management by Annina Schmid, Joel Fundaun and Brigitte Tampin. It’s great, obviously.
* Patient-facing interview with me on The Back Pain Podcast. I think this went pretty well. I hope it’s useful to share with patients. The one caveat is I talk about disc herniations a lot, so it might not be relevant to every patient (I should do a future newsletter on the different structural causes of lumbar radicular pain…)
* Transcripts are coming of all pods… but it doesn’t half take a while
* I couldn’t think of any pictures to illustrate this newsletter so here are a couple more from our road trip instead… 🤷
Til next time!
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Hello and welcome to the sixth copy of the newsletter!
In my TherapyLive talk I pitched that when we treat radicular pain we should think in terms of nerve health and sensitivity rather than nerve compression (although the former includes the latter!). To illustrate what I mean by "nerve health" I showed pictures from a study by Albrecht et al. in which the authors image neuroinflammation in people with chronic radicular pain. The first picture is cool but not unexpected: the green arrow points to a small patch of yellow in the intervertebral foramen which represents neuroinflammation (or, more accurately, a marker of neuroinflammation).
We have known for some decades that lumbar disc herniations are pro-inflammatory to the surrounding tissues and that this probably drives a lot of acute "radiculitis". In fact, Albrecht was a bit surprised that the signs of neuroinflammation in the foramen were not stronger and more consistent. Maybe it's because the participants in his study had chronic, not acute pain.
The second image is less intuitive: run your eyes down the aggregated images of the spinal columns of the control patients and the patients with radicular pain and you will see that there is more of a yellow hue to the spinal cords of patients with pain.
Although these patients have (or have had) an insult to the nerve roots in their lower lumbar spine, they also have neuroinflammation in their spinal cords, in the lower thoracic and upper lumbar spine. The neuroinflammation has "spread". In cross section, it is more clear.
Whenever I show this image a few people will message me afterwards saying how striking it is. So there is something important here that I want to "zoom in on". And my main stumbling block is, what on earth is neuroinflammation?
This week’s podcast
This week's podcast is an interview with the lead author of the study, Daniel Albrecht (pron. Albright). Dan speaks really well on this subject. In the podcast, he describes the basics of neuroinflammation and the findings of this study. He also takes on the trickier questions that surround this topic and makes it clear what we know and what we don't know. It’s on all major platforms if you search for “The Sciatica Podcast”, or you can click through from this email. Do listen!
Okay, what on earth is neuroinflammation?
Neuroinflammation is not necessarily pathological
The first thing to say about neuroinflammation is that it is not in itself pathological. Just like inflammation in the muscles, joints and skin, inflammation in the nerves arises in response to dangerous stuff like pathogens or tissue damage. Many different cells and molecules work together to limit the danger and repair any harm done. Neuroinflammation only becomes a clinical problem when there is too much of it, or it goes on too long.
Neuroinflammation is a continuum
The second thing to say is that it is not really something that is turned "on" or "off". We use words like "activated" to describe microglia, which makes this confusing. But really it's a "more" or "less" process, not "on" or "off".
At one end of the continuum, transient, low level immune signalling is involved in the normal development of memory and learning and arguably doesn’t qualify as “neuroinflammation” at all. At the other end "very rapid and dramatic" neuroinflammation kicks in after serious nerve injuries.
What’s involved?
Now let's introduce the "characters" of neuroinflammation to tell the story in stages. To me, one of the most challenging aspects of understanding neuroinflammation (to the extent that I have) was wading through the many and various cells and molecules which all seem to do subtle variations of the same thing. For clarity's sake, I have cut out a lot of these (sorry, fans of TLR-4) so that I can tell a coherent "story" within the scope of an email newsletter...
Glia
Glia comes from the Greek word for "glue" because for a long time, it was thought that that's all these cells are. It is only since the 1990s that scientists have begun to appreciate that they have an important, active role in how the nervous system works. The two important types of glia for us are microglia and astroglia.
Microglia
Microglia are the first to respond to a nerve injury. They reside in the CNS and they look like this (like octopuses).
Image via
They are not connected to each other. They each have their own domain. Their octopus legs are constantly "feeling" their environment, looking for threats. They support neurons, tweaking their synapses, keeping them healthy and clearing away any debris.
Microglia are "activated" by anything that might mean danger. This could be a nerve injury, including a peripheral nerve injury, but it could also just be a lot of nociception. That said, they are much more reactive to nerve injuries than, say, peripheral inflammation. When activated, microglia pull in their octopus arms and increase in size so that they look like "fat, angry rainclouds"
They express different surface proteins, ready to get to work. And they proliferate and move to the site of danger and other related parts of the spinal cord and brain.
Again, microglia activation is not an accident or a pathology, it is an adaptive response to danger. They are "looking for" danger all the time. And, so they don't miss it, neurons release signalling molecules to "tell them" to activate.
How does this lead to pain?
Activated microglia express proteins that are responsible for releasing inflammatory cytokines (signalling molecules). If you are anything like me, this is where your eyes might start to glaze over. It just becomes a list of things you have no mental image for: TNF-a, IL-1B, BDNF...
I think the fear is that if you forget for a second what, say IL-1B does to GABA then you will miss some vital piece of the puzzle. Luckily, according to the researcher Ru Rong Ji, although the bits and bobs involved in neuroinflammation are diverse, they "modulate pain in surprisingly consistent ways". Essentially, Ji says, cells like microglia "release neuromodulatory substances [the TNF-a, IL-1B, BDNF etc. etc.] in close proximity to nociceptors which either promote or dampen pain depending on the specific identity of the mediators involved". If the balance of these neuromodulatory substances is in favour of those that are pain-promoting, then neuroinflammation is more likely to contribute to pain. (We will come to the pain-dampening ones later...)
Astrocytes
This frenzy of microglia activation is usually short lived. It is probably more involved in acute pain. But, microglia will signal to astrocytes which are slower to activate but more persistent. (This is partly why neuroinflammation is often considered a factor in chronic pain states, while classical inflammation is not.)
Astrocytes look like this.
Like stars, as their name suggests. They are connected to each other, in a fine, fibrous network. This network enwraps synapses (as many as one million per astrocyte) and connects with blood vessels. When activated, astrocytes change their normal, run-of-the-mill communications with neurons and instead tell them to produce more neurotransmitters and inflammatory cytokines.
Immune cells
Astrocytes also contribute to another important feature of neuroinflammation: the blood-nerve barrier, including the blood-brain and blood-spinal cord barriers, becomes more permeable. (It seems that nociception also contributes to this change.) This allows immune cells like macrophages (in the PNS) and t-lymphocytes to more readily enter the neuron itself. Here’s a T-lymphocyte.
And here’s a macrophage.
Again, this is generally a good thing as it allows these cells to go to work and clean up debris and damage following injury. But, an unwanted consequence of this is damage to the nerve itself: for example, demyelination and axon degeneration. And, as Ji observed, immune cells also modulate pain in a manner similar to other non-neuronal cells, including the glia: they are capable of producing mediators that promote or dampen nociception in the neurons around them.
Interactions
By now, you might have noticed that neurons and microglia "talk to" each other. And more broadly, the sensory and immune systems also "talk to" each other. There is bidirectional signalling. To me, it is not that hard to get the idea of cells and molecules sensitizing a nociceptor. It is a bit less obvious that the nociceptor also takes part in the conversation. That is, nociceptors modulate inflammation. They too can express cytokines and trigger inflammatory cascades. They are not just wires but actively take part in the feed-forward mechanism of neuroinflammation.
Resolution
How does this all end? You might think that neuroinflammation kind of fizzles out. In fact, like classical inflammation, it is resolved by an active process. This process has another list of confusing molecules (cytokines like IL-4, IL-10, IL-13, TGFB and things called resolvins and endocannabinoids) but this time, they are anti-inflammatory. Microglia and nociceptors, too, release anti-inflammatory mediators.
Some researchers think that many chronic pain states might be a failure of this resolution mechanism.
To summarise…
So, let's bring this back to the people with radicular pain who participated in Albrecht's study. Now we have added some texture to this term "neuroinflammation" we can *tentatively* say something like this:
The study by Albrecht et al. shows that some (but not all) people with chronic radicular pain have ongoing, increased levels of neuroinflammation in their peripheral and central nervous systems. In these patients, peripheral nerve injury and ongoing nociception activated microglia in the spinal cord. These microglia released mediators which increased the excitability of nearby neurons, and reduced their inhibition. They also helped to trigger the activation of astrocytes, which have a similar but longer-lasting role. Other non-neuronal cells such as macrophages and t-lymphocytes may have migrated to these neuro-inflamed areas and crossed the blood-spinal cord barrier to infiltrate neurons themselves. All this became a feed-forward mechanism in which non-neuronal cells make neurons hyper-excitable, and hyper-excitable neurons also activate non-neuronal cells. Under normal conditions, an active process involving anti-inflammatory mediators should resolve neuroinflammation. But, for the participants in the study by Albrecht et al., it seems this has not happened, or is yet to happen.
That’s the end of the newsletter for this week! I had originally intended to talk more about the clinical significance of this, particularly when it comes to exercise. But I have already broken my promise to keep these newsletters short. I will leave that for a future edition…
I have added a few of the best papers I found to this google drive folder.
Please let me know if there are any errors or important additions. And do listen to the podcast with Dan, where he goes into more depth on his study and also delineates what we know and what we don’t know about neuroinflammation and pain…
Til next time!
Tom
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Hello everyone!
Welcome to the fifth copy of the newsletter.
I was delighted to speak with David Butler a couple of weeks ago about nerve root pain. With his permission, I recorded our chat so everyone could listen. And then I realised I’d started a podcast!
I’ve avoided the temptation to give it a cringey pun title and just gone with “The Sciatica Podcast”. This will be the first of many episodes. I’ll be speaking with experts in the field and people with sciatica. And I think it would be a nice idea too to have the odd journal club or case study; do get in touch if you want to be involved with those.
As you can see, you can listen to my chat with David in this email. By searching for “The Sciatica Podcast”, you should also find it on Itunes, Spotify etc.
It’s a great chat with David, I think. My main goal going into our conversation was to find new perspectives on a topic that David has already written so much about. I think we succeeded.
In other news,
* I spoke at TherapyLive on the topic “5 Simple Things We Can Do To Improve Care For People With Sciatica”. I proposed:
* We take our time during our assessment to help the person with radicular pain to understand what is going on, using simple language to explain what are often unusual symptoms.
* We set the right expectations early on, not implying that acute nerve root pain will inevitably get better in a couple of months or so.
* We straight away explain the conditon with reference not only to mechanical compression, but also nerve sensitivity.
* We shouldn’t be referral-shy when people have severe acute sciatica (something David and I discuss in our podcast).
* We forget about spinal stability and frame our exercises as improving nerve health, instead.
The talk is available as part of a bundle with the other talks on Therapist Learning.
* I had an enjoyable, quite rambly and discursive chat with Oliver Thompson on the Words Matter Podcast.
* This edition of the newsletter is late because I couldn’t quite get it out before we moved house at the end of last month. We just made a big road trip from Michigan to California to stay with family, and in a month or so we will be driving East again to Texas to settle in Houston!
* Although it probably doesn’t make much sense given that I’ve just posted a monthly newsletter more than one week late, I’m planning to make this newsletter weekly now. Weekly, but much shorter! They are probably way too long at the moment for most people to digest. So I’m going to try to make them more focused, but more frequent, from now on.
Which means I should probably sign off now!
Til next time,
Tom
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![The mechanisms of radicular pain, with Annina Schmid [Repost!]](https://is2-ssl.mzstatic.com/image/thumb/Podcasts115/v4/36/c7/12/36c712f3-3774-e742-e025-56cc6c0e53c3/mza_1212035900332492233.jpg/80x80bb.jpg)