Bug or Feature? SAT edition

A few weeks ago there was a Less Wrong thread about truly brilliant people, especially mathematicians, who often got good but not perfect SAT scores.  The consensus was that the SATs were a better test of how long you can go without making a mistake than of genius.  At the time I read this I (who got good but not perfect SAT scores) was all “yeah, the SATs are bad at measuring brilliance.  And I did better in more advanced classes than I did in the intro ones, because the intro ones were about how close you came to matching their expectations, and the advanced ones were about original thought.  In fact the smartest people will do worse, because this is so trivial to them it is boring.  I sure hope the SATs feel bad for failing to recognize my their brilliance.”

I was about 10% of the way through Safe Patients, Smart Hospitals when I realized that if I am recovering from dangerous surgery and need a central line*, it is more important that my doctor can follow the safety checklist without getting bored than that he be capable of original thought.  Like, way, way more important.  We need doctors capable of original thought somewhere, so they can invent new procedures and drugs and things, but outside of their magesteria they do more harm than good.

dr_house_brain
Gregory House would be terrible at inserting central lines. That’s why he has Taub.

So maybe the SATs are doing a valuable service by injecting a little bit of what it takes to succeed in the real world into their otherwise-pretty-much-an-IQ-test.  And maybe we should start selecting doctors for what they actually do most of the time.  Alternately, maybe we should move central-line-type work to techs and computer algorithms and use doctors for research and cases weird enough to be on TV.  But what we should definitely not do is select people for brilliance and make lives depend on their ability to work methodically.

*Central lines deliver fluids better than IVs but are more vulnerable to infections, which can be fatal, especially in people recently weakened by trauma or illness, which is everyone who is getting a central line.  You can greatly reduce the chance of an infection by following a fairly simple list of steps like “use gloves” and “sterilize skin”, but these are often skipped.

Review: Selling Sickness ( Ray Moynihan, Alan Cassels)

(Previously)

Selling Sickness‘s goal was to convince the reader that pharmaceutical companies manipulate perception to create an impression of disease where none exists.  I was going to say it failed, but no, it didn’t.  It actually has some pretty good examples of how pharma manipulates perceptions.  I just find it’s own view problematic as well.  E.g. Pharma is trying to make the diagnosis of Female Sexual Dysfunction equivalent to male impotence, when it clearly isn’t, and that’s bad.  But Selling Sickness’s  implication that the components of FSD (low libido, anorgasmia, pain during intercourse) should not be taken seriously by medics is ridiculous.  Sexual pleasure is important to many people in its own right, and any of those issues could be a symptom of a serious underlying problem.  Testosterone is a bad treatment for low libido because it’s a major hormone with far reaching effects, but it is an excellent treatment for low testosterone, a serious health problem for which low libido may be the most obvious symptom.

Selling Sickness talks about how pharma companies manipulate disease definitions (by sponsoring educational conferences and key decision makers), but it doesn’t explain anything else about how those decisions are made, or what would happen in the absence of pharma money.  Without that information it’s hard to draw conclusions.  Which I guess is how I feel about the book as a whole: its advocating a very specific point of view rather than informing you on the topic as a whole.  There’s nothing wrong with that, except that it (rightly) condemns pharmaceutical companies for doing the same thing.

*Obviously there’s a lot of variation and some doctors respond to those symptoms properly.  My sense from the literature and anecdata from my friends is that they’re going against the grain when they do so.

ETA: Slate Star Codex provides an example of pharma criticism done right, because he talks about the cracks in the system capitalism is filling.

Selling Sickness: Depression and Anxiety

Previous: Aceso Under Glass Valentine’s Day Special

Like many people, the authors of Selling Sickness believe that drugs for depression and anxiety are over-prescribed, that they are used to escape everyday emotions, and that this is terrible.  Again, I wish they’d defined their terms better.

For example, it sounds ridiculous to give someone Prozac because they’re sad their mom died.  That sadness is categorized as natural and healthy, in fact barring very unusual circumstances it would be viewed as sick not to feel sad at that point.  But you only get anti-depressants for “being sad” if it lasts more than two years.  Until then, anti-depressants are given only when negative emotions* start destroying a person’s ability to run their own life, and thus become self-reinforcing.  It’s completely natural and healthy to still be morning your mom’s death two months later, but if you’re unable to shower or eat for that length of time it doesn’t matter that the depression has an obvious external cause, it’s hurting you and there shouldn’t be any shame in accepting medical treatment for that.

A common fear I hear around anti-depressants is that they make people tolerate situations which should be depressing, and thus impede their exit.  That’s a real concern, and I think we should watch for it.  On the other hand, there are lots of people who want to leave but are unable to do so because they’re so depressed, and anti-depressants give them the activation energy and hope in the future that lets them leave.  And the same drug can have both effects in different people, or even the same drug at different times, because humans are weird and we don’t understand what we’re doing.

“We don’t understand what we’re doing” is not a great endorsement for something that’s screwing with the chemicals inside your brain.  I do think we need to use caution, that the risks are poorly understood, especially by GPs, and that nutrition and exercise are underutilized as treatments.  I also think that even when anti-depressants are the best individual decision, mass use of them can indicate a problem (I’ve heard 50% among PhD students, which cannot be okay).  And there will always be room for debate- should you be expected to work productively a month into grieving?  To work in a really difficult, dehumanizing office environment?  Would you need anti-depressants to take care of your kids if you had better community support?

But big pharma is not the one creating those societal conditions, and destigmatizing mental illness because it benefits them financially seems like a success story to me.  If we’re going to counter over prescribing let’s look closer to the problem (doctors) or further away (societal structure), not question the people receiving needed help.

*Not necessarily sadness.  In fact in men depression often manifests as anger, which leads to under-diagnosis.

Aceso Under Glass Valentine’s Day Special

My original plan was to finish Selling Sickness and write an overall book review, but I have reached that stage where I can’t continue reading it until I get some of my current thoughts out of my head, so we’ll be doing this in stages.

There exist many, many criticisms of the pharmacutical industry, all of which I dislike for framing it as the fault of the pharmaceutical companies and not the FDA.  If you want to learn more about this, Bad Pharma is a good source.  Selling Sickness‘s is more specifically about claim is that pharmaceutical companies deliberately manipulate both the public’s and the medical field’s view of illnesses, and “defines health people as sick” for their financial benefit.

I really, really wish Selling Sickness had defined its terms better.  Let’s use heart attacks as an example, because it is Valentine’s day.  No one questions that heart attacks are extremely bad, that they are associated with high blood pressure and high cholesterol, and that giving medications that lower blood and cholesterol to people who have already had a heart attack lowers the chance of a second one and increase life expectancy.  From this some people concluded that high blood pressure and cholesterol cause heart attacks, and we should lower them with drugs even in people who have never had a heart attack.  Selling Sickness describes that as turning healthy people into sick people.

Let me say out several different possibilities that would account for all available information:

  1. High blood pressure and/or high cholesterol damage your coronary system, causing heart attacks.
  2. Sufficiently high blood pressure and/or high cholesterol damage your coronary system, causing heart attacks, but we have drawn the cut off in the wrong place.
  3. High blood pressure and/or high cholesterol damage your coronary system, causing heart attacks, if and only if you have already had a heart attack.
  4. High blood pressure and/or high cholesterol and heart attacks share a root cause, the common treatments treat that cause, and the indicator numbers go down as a result.
  5. High blood pressure and/or high cholesterol and heart attacks share a root cause, the common treatments treat only the symptoms and leave the chance of a first heart attack unchanged, but coincidentally help after a heart attack.
  6. There are multiple causes of high blood pressure and high cholesterol have multiple causes, one of which also causes heart attacks.  Drugs happen to attack root cause if you have it, lower blood pressure and cholesterol to no effect if you do not.
  7. High blood pressure and/or high cholesterol damage your coronary system only in conjunction with an unidentified third factor, and so drugs reduce lifetime mortality if and only if you have that factor.  People who have a heart attack have that factor by definition and thus benefit from blood pressure/cholesterol medications.  They would benefit from them before their heart attack as well, but we have no way to identify them ahead of time.

Under which of these scenarios would you call someone with high blood pressure sick?  It’s a trick question because sick and healthy aren’t actually medical terms. The term for something given to an asymptomatic person that keeps them from developing symptoms in the future isn’t “making them sick”, it’s  “preventative medicine”, and it’s generally considered a good thing.

If high blood pressure and cholesterol don’t immediately cause symptoms but do damage your coronary system, taking drugs to combat them is a good call (dependent on side effects).   You could call them sick or not, it doesn’t matter.  If there was a pill that kept you at your physical and mental peak for 100 years you’d take it, even if your only health condition is being mortal.  Or maybe high blood pressure/cholesterol does indicate illness, but for one of the reasons outlined above, medication helps the numbers without improving symptoms or outcomes.  Then you’re sick but shouldn’t take medicine.  How useful medicine is has nothing to do with the English words “sick” and “healthy'”.

To be fair, researchers make the same mistake.  What we ultimately care about is if medication improves an individuals quality and quantity of life (with exact weightings dependent on the individual).  That takes a long time to do because people take forever to die.  You only get 20 years total from when you first register the molecule.  For a drug intended to prolong life given to people in their 50s, the drug could go off patent (destroying any ability to recoup the cost of the trials) before it got out of trials.   Even waiting for heart attacks takes a very long time and a very large sample size,because heart attacks aren’t actually that common.  So researchers use proxy measures like high blood pressure and cholesterol, on the assumption that anything that lowers those must prevent heart attacks.  Even researchers who aren’t trying to recoup financial costs do this, because they would like to produce results some time before they retire.  The problem is that even if high blood pressure and cholesterol are tightly coupled with heart attacks, this method will inevitably over-include things that somehow affect the proxy measures without affecting heart attacks, and miss things that decrease heart attacks or lifespan without affecting the proxy numbers.  And of course it’s entirely possible the FDA let pharma companies nudge the cut offs for treatment much lower than they should be, because that’s easy.

So yes, there are a lot or problems with aggressively treating proxy numbers, but “applying the sick label to healthy people” isn’t one of them.

Anticholinergic agents and dementia

A new study came out this week suggesting use of a particular class of drug after age 65 was associated with dementia.  Here’s what you need to know.*

The study is retrospective, meaning it took people who developed the disease of interest and then looked backwards at their medications.  Retrospective studies are prone to a number of problems, the biggest one being that even young people with healthy memories are crap at giving you their drug history over the past 10 years, and this is a study of people with dementia.  The researchers dodged this by using an HMO database of the subjects complete medical history, which is a neat trick.  The second problem is that retrospective studies can easily end up being painting the bulls-eye after they’ve fired the arrow.  Mere chance dictates that if you track enough traits, any random subset of a population is likely to have something more in common with each other than with the rest of the population.  If you use the traditional bar of statistical significance (5% chance of results arising by chance), checking 20 traits gives you an expected value of 1 false positive.  To be fair, this study has a much higher significance level, and the effect was dose dependent, which is a very good sign that it’s legit.  The authors heavily imply they deliberately studied anticholinergics rather than shotguning it, but without preregistration there’s no way to be sure.

Anticholinergics come in two forms: antimuscarinics, and antinicotinic.  Short version: these work on different types of neuroreceptors, which live in different parts of the body and do different things . Every example drug they give is an antimuscarinic and of the classes of drugs they list, many have no antinicotinic members.  Even if they technically included antinicotinics in the analysis, they would be such a small portion of the sample that their effect could be overwhelmed.  So I don’t think you can apply this study to drugs like bupropion, which is an antinicotinic.

I don’t like the way they calculated total exposure at all.  Essentially they counted the normally recommended dose of any medication as One Standardized Daily Dose.  But those dosages vary wildly (even the examples they give span an order of magnitude), as do the particular drugs’ ability to cross the blood-brain barrier.  The drugs are prescribed for a huge variety of causes, and what’s sufficient to stop incontinence has nothing to do with what’s sufficient to slow Parkinson’s.  This oversight may cancel out with the fact that they created buckets of dosages rather than do a proper linear regression, in the sense that low-def pictures cancels out bad skin.

The obvious question is “but maybe the same thing that drove people to need anticholinergics increases the likelihood of dementia?”  This study has a much better retort for that than most, which is that anticholinergics were prescribed for a variety of causes, and it’s unlikely they all correlate with dementia.  I find that explanation extremely satisfying, except that they only evaluated the drugs as a single unit.  Antidepressants make of over 60% of the total SDDs taken.  The next most common is antihistamines at 17%.  But since more than 60% of the population took at least one SDD, it seems likely that those were taken intermittently, as opposed to the constant drip of antidepressants.  This leaves open the possibility that the entirety of the effect they attributed to anticholinergics was in fact caused by tricyclic antidepressants alone- and that the real culprit was depression.  The obvious controls were to evaluate the anticholinergics separately, and to compare rates of dementia among TCA treated patients with those treated with other antidepressants.

The subtler version of this question is “what if anticholinergics prolong life, giving you more time to develop dementia?”  I don’t see anything where they checked for that either way.  They did ask for people’s perception of their own health, and that was negative correlated with TSDD, but if TSDD is correlated with depression it’s hard to know how to interpret that.

For all those criticisms, this is an amazingly strong result for a medical study**.   No one study can prove anything (even if i think they had the data to do more than they did).  It definitely merits further investigation (ideally some with animal models, so we can do the causality experiments that would be super unethical in humans), and maybe even behavior change in the meantime, although a lot of the drugs studied are already obsolete or second line.  Plus it another piece of data that will help us figure out how to fight dementia, and that makes me really hopeful.

*Read: here’s what I learned.

**Yes, this should worry you.

Loratadine for Allergies?

The Decision Tree casually describes loratadine (brand name: Claritin) as barely better than placebo for treating allergies.  This is news to me because Claritin was absolutely critical to me graduating middle school.  If I forgot to take it in the morning my mom had to drop it off at school by lunch.  Without it I slept 16 hours a day,* woken up only by hives that itched so intensely they burned.  This isn’t actually relevant to me now because my allergies were taken care of my unprocessed honey and moving, but I couldn’t believe something once so important was essentially a sugar pill. So I investigated.

First stop, Wikipedia, which definitely backed my claim that Claritin treated sneezing, runny nose, itchy or burning eyes, hives, and other skin allergies.  But of 19 citations, 5 were unavailable to me (either they were books or in languages I don’t read), 13 were on topics other than clinical efficacy (e.g. side effects or mechanism), and 1 had a sample size of 192 and was a comparison against another anti-histamine, with no placebo or no-treatment group.

So I checked google scholar, where I found numerous minuscule studies (n = 14, 7 treatment groups) in which loratadine was better than placebo but worse than other drugs in the same class.**  If that’s true, why did loratadine get so much more attention?  I looked up the other drugs, and it turns out that some of them (cetirizine/Zyrtec) had similar efficacy but came out later, and went over the counter later as well.  Others (Terfenadine/Seldane) had much uglier side effect profiles (e.g. cardiac arrythmia if you eat a grapefruit).  So Claritin’s advantage seems to be being the first drug to market that treated the problem with minimal side effects.  I also wonder if Decision Tree‘s author (Thomas Goetz) was looking at a particular symptom set?  For example, loratadine appears to do well as a treatment for hives but there are better options for hay fever.

Some people suggest that having multiple drugs with similar response rates in the same class on the market is some sort of failure.  They are wrong and they should feel wrong.  First, these drugs were developed in parallel by different companies. While all the ones we heard of worked out, very few chemicals that pharma companies research become prescribable drugs, and they can’t predict which ones will do so ahead of time.  What if McNeil stopped researching Zyrtec because Bayer was researching Claritin, and Claritin made you grow arms out of your face?  We’d have lost years of allergy relief.  Second, the fact that they had similar average efficacy and side effects doesn’t mean they have the same effect in every person.  People are squishy and they don’t make sense, and differing reactions to drugs is one of the milder ways this manifests.

*No, fatigue is not a normal symptom of allergies, but I got it most springs and it went away with anti-histamines, which is good enough for a field diagnosis of allergies.

**I also found a lot of studies detailing the effects of loratadine in conjunction with another drug, mostly montelukast, and abstracts that reported loratadine’s efficacy relative to older antihistamines but without absolute numbers.

Review: The Decision Tree (by Thomas Goetz)

My trail of discovery to The Decision Tree was as follows:

  • Discover Iodine’s in-browser medical translator, become fan for life.
  • Watch Iodine CEO’s (Thomas Goetz) TED talk on the problems with how medical information is currently presented, and his solution.  Become very impressed.
  • Discover Goetz has a whole book on this stuff.  Order from library.

This was maybe not have been the best order to do it in.  Decision Tree is really, really good, but it lacks the specificity of the TED talk or Iodine’s recent work.  If I’d read it first, the other work (which was produced later)  would have been fulfilling the promise of the book.  But reading it last, I kept waiting for the other shoe to drop.  It is an amazing launching pad, but I went in expecting to see what had landed.

That may not even be fair.  Goetz points to a lot of specific things, like the Quantified Self movement, PatientsLikeMe.com, and actual research on how Dr. Internet affects people.  It’s just that none of these so singularly improve the signal to noise ratio the way Goetz’s work on presentation of test metrics did.  I guess what I’m saying is you should watch that TED talk.

Now that I’m over the fact that Decision Tree is not a 250 page TED talk, I can appreciate it for what it is, which is a reasonable 101 text on the concept of individuals monitoring and improving their own health.  It doesn’t give many specifics for either of those because the answers are so specific and so personal, but it does leave the reader better prepared to evaluate possible solutions they find.   That’s actually pretty hard to do, and really useful.  I could also see it as useful for medical professionals who are on the fence about patient-driven care.*  It is extremely helpful in explaining why over-testing is so dangerous, while respecting individuals’ right to data.  And if you’re not reading it during or immediately after a painful, stressful medical procedure, it’s actually a pretty light read. So if this book looks interesting to you I’d recommend it.

*Goetz is unreservedly pro- patient led decision making and research.  I am too, until I remember a lot of the anti-vaxxers have put an enormous amount of research into their idiotic, dangerous, anti-social position.  I don’t know how to preserve the rights of me + my friends to know our own data and correct our doctors’ mistakes while preserving the rights of children to not die of entirely preventable diseases.

The Kitten Pain Scale

I very briefly flirted with Quantified Self and then jumped off the bandwagon because it was making my personal signal:noise ratio worse.  But my neuroendodontist* has given me several drugs, and he wants to know how they work.  Allow me to give you a brief list of things that make measuring this difficult

  • Treatments are all on varying schedules- some daily, some daily with a build up in blood stream leading to cumulative effects, some as needed to treat acute pain, some on my own schedule but hopefully having longer running effects.  Some are topical and some are systemic.
  • I have several home treatments like tea and castor oil.  I’m not going to not take them in order to get more accurate assessments of the drugs, both because ow and because pain begets pain.
  • Taking treatments as needed + regression to the mean = overestimate of efficacy.
  • Pain is affected by a lot of non drug things: sleep, stress, temperature, how ambitious I got with food, amount of talking, number of times cat stepped on my face in the night, etc.
  • We are hoping some of these drugs will work by disrupting negative feedback loops (e.g. pain -> muscle tension -> pain), which means the effect could last days past when I take in.  In the particular case of doxepin it might have semi-permanent effects.
  • Or I could develop a tolerance to a drug and my response to a particular drug will attenuate.  That is in fact one reason I was given so many choices as to medication: to let me rotate them.
  • We have no idea how these drugs will interact with each other in me.  We barely have an idea how the interact in people in general.
  • If I believe something will help my pain will lessen as soon as I take it, long before it could actually be effective.  Not because I’m irrational, but because my brain reinforces the self-care with endorphins, which lessen pain.
  • At the same time, having more pain than I expected to feels worse than the exact same pain level if it was anticipated.
  • Side effects: also a thing.

“I think I feel better when I take this one” was not going to cut it.

Then there was the question of how to measure pain.  Ignoring the inherent subjectivity of pain, neuralgia is a weird beast.  I already hate the 1-10 pain scale because pain has threshold effects and is exponential.  I could create a single pain number at the end of the day, but my pain is not constant: it spikes and recedes, sometimes for reasons, sometimes not.  What I would ideally like to track is area under the curve of pain**, but that requires polling, which would create horrible observer effects.  If I ask myself if I’m in pain every 15 minutes, I will increase my total pain level.  I could poll less often, but the spikes are random and short enough that this was not going to be accurate enough to evaluate the treatments.  I could count pain spikes, but that ignores duration.  Determining duration requires polling, so we’re back where we started.  I could deliberately poke a sore spot and see how bad the resulting pain is, but

  1. Ow
  2. A treatment that doesn’t affect sensitivity but does keep me from spontaneously feeling pain because the nerve is bored is a success.  If we wanted me to be numb we would do that.

It’s just really hard to measure something when your goal is for it to be unnoticeable, and measuring it creates it.

So I came at it from the other side.  What happens when pain is unnoticeable?  I enjoy life more and I get more things done.  Could I measure that?  Probably.  They have the bonus of being what I actually care about- if something left me technically in pain but it no longer affected my ability to enjoy or accomplish things, that would be a huge success.  If something took away the pain but left me miserable or asleep, it is not solving my actual problem.**

So one metric is “how much I get done in a day”.  Initially this will be the first number between 1 and 10 that I think of when I ask the question at the end of the day, but I’m hoping to develop a more rigorous metric later.  You’d think enjoyment of life couldn’t ever be rigorously measured, since it’s so heavily influenced by what is available to me in a given day, but I say that brave men can make it so.  And so I introduce to you: the kitten pain scale.  Kitten videos vary a little in quality, but I think my enjoyment of any single video reflects my internal state more than it does the video. Three times a day (shortly after waking up, shortly before screen bed time, and sometime mid-day that can vary with my schedule but must be selected ahead of time to avoid biasing the data), I will watch a cute kittens video and record how much I enjoy it.  The less pain I am in the more I should enjoy the video.  This will give me a (relatively) standardized measure of pain without risking inducing it.

This is still not what you would call a rigorous study.  An individual choosing what to take among known options never will be.  But I seriously think the kitten pain scale could be a contender to replace the stupid frowny faces.  My first draft is available here.  Right now it’s set to measure over the course of a day, because that’s the scale I expect from these meds, but you can add bonus measurements at set times after taking meds if you like.

Possible additions: cups of tea drunk in day.  Right now that seems like too much work to measure, but when tea is available it’s a pretty good indicator of how much pain I’m in.

*I am still angry that I know what that is, much refer to one using possessive case.  But given that, I am extremely grateful I live within biking distance of a world class research facility in the discipline.  Even if the physical facility could be a case study in how economic insulation leads to bad user experience.

**This is why none of my treatment options are opioids.  Strong ones technically reduce pain, but they also leave me miserable.  The fact that some people take them for fun is all the proof of human variability I could ever need.

Adventures in Dentistry and Neurology

I forget if I mentioned it, but I had nerve damage from the first dental surgery, way back in June.  Everything else healed up more or less all right, but that one kept hurting.  Actually it felt like two damages- one that was healing, albeit slowly, and one that was staying static or getting worse.  The prospect of living with that pain for the rest of my life was really daunting.  Medical marijuana, which had been so helpful at first, was having more side effects with fewer desirable effects every day.  It eventually became clear my surgeon had no idea what was going on or how to fix it so I went to a neuroendodontist, a subspeciality I really wish I wasn’t already familiar with.

toenailectomy looks awful but feels like nothing at all.  A neuroendodontal exam is the exact opposite.  It looks like some guy very gingerly touching around your mouth, but he is not only deliberately provoking pain, he needs you to pay attention to the pain and report on in it excruciating detail, while you remind yourself that inaccurate reporting leads to inaccurate diagnoses.

For all that pain, I actually got very good news.  Even though it feels like I have two distinct damages, it’s actually only one, and it is healing.  Nothing is guaranteed in neurology but existing data is consistent with this eventually healing itself.  And in the meantime, he gave me new and different medicines.  We’ll see what the side effects are, but at the very least I have options to rotate through.

Adventures in Podiatry and Neurology

WARNING: THIS ONE IS GRAPHIC EVEN BY MY STANDARDS.  NEEDLES, PAIN, AND TOENAILS.

Recently I learned toenails aren’t supposed to be under the skin of your foot and hurt constantly; this is an ingrown toenail and it’s a solvable problem.  By “recently” I mean a year and a half ago, but a little pain when I flexed my toes in a shoe did not seem as important as the pain in my mouth or my inability to digest food, so I only got around to seeing a podiatrist now.  If you develop an ingrown toenail there are home treatments to coax it better, but if you’ve always had it the cure is a little more drastic: they cut off the bit of the nail that has grown under the skin and cauterize the nail bed so it never grows back. If you are curious, here’s a video of the actual medical procedure:

The worst part is the lidocaine injection. There’s a topical anesthetic, but they root the extremely thin nail around under your skin in order to find the nerves and inject directly over them. The podiatrist will describe it as slightly painful, but they are lying, and it will make you doubt them when they promise the rest of the procedure is painless. That part turned out to be true: with enough lidocaine you genuinely can’t feel them slip the scissors/pliers under the nail bed, or the burny stuff*, unless you are a freak who processes -cain very quickly, in which case they will give you more and it will stop hurting.  But the anesthetic injection was pretty brutal.

That is not actually the interesting part. In between the lidocaine and the scissors/pliers, they test your numbness with what looked like a large blunt toothpick. My podiatrist, which more flourish then was strictly necessary, brought it down from a great height onto my toe.

I screamed.

Then I realized it didn’t hurt at all. My brain had combined the memory of the painful needles and the visual information about incoming sensation and preemptively sent a scream response before it noticed I couldn’t feel anything. I never had quite that strong a reaction again, but there was an extremely weird dissonance as I watched something I knew should hurt, yet got only vague reports of pressure from the area.

This works in reverse too.  Phantom limb syndrome is a condition in which people missing a limb (even one they never had) experience excruciating pain where their brain thinks that limb should be.  One of the only effective treatments is mirror therapy, where a mirror is used to simulate the appearance of the missing limb, and somehow the brain goes “oh, I guess it’s fine.”  This clip from House is not quite as accurate as the matrixectomy one (mirror therapy rarely involves kidnapping), but the science is sound.

The lesson here is that even something that feels incredibly simple and real, like pain, is in fact an artifact of post-processing on several different inputs.

*Dr. Internet says phenol but I could have sworn it started with an M. In my defense, he gave me the proper name after the needles bit and I was fuzzy.