The Sciatica Podcast

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 on…

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 t…

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

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!

Lectures for clinical teams

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

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…

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

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

Lectures for clinical teams

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