Several months ago I announced an RCT I was running for a client to test ketone esters as a nootropic. After many more months than planned (pro-tip: do not create a study that depends on people with ADHD following a finicky multi-step process, and if you must, make your ops perfect) I failed to find an effect of ketone esters on productivity. It was a small study and a lot went wrong so this failure isn’t conclusive, but since I expected to find an enormous effect size, I’m still pretty disappointed.
I originally intended to write up detailed results and a post-mortem on experimental operations. I’m unfortunately pressed for time right now, and can’t work up the motivation to detail exactly how little effect ketone esters had. If you’re considering running your own experiment and want the details, please reach out here or over email; I’m happy to share if it will be useful, but I didn’t want to delay publishing over details that probably don’t matter. However, you can see the experimental protocol in detail here. If you check, the hash of that file matches the hash in the recruitment doc.
The overall outcome: if you compare the average productivity for control and treatment days per person, and then average the per person difference together, that average is -0.2 (scale of 1-10), meaning treatment made people slightly worse on average. If you include only people who completed more than 10 of the planned 14 observations (4 out of 7), the average improvement is 0.3 (same 1-10 scale). The largest improvement for any one person was 1.1. I didn’t bother to check for statistical significance because even if it eked out a p-value, the real-world significance is too small.
This result is confusing, because ketone esters obviously work really well for me, and a few other people I know. That could be a placebo, but the effects are so strong and consistent that that seems unlikely. It’s possible there was an experimental error – our operations were really not what they needed to be for a study of anyone, much less people specifically selected for having difficulties with organization – but even if I squint at the data I can’t see the kinds of patterns that might hint at that. Or the design could have been flawed; I was trading off ideal circumstances and ease of use for volume of participants.
Given these results, I intend to keep taking ketone esters when they feel helpful to me, but can’t recommend them as in any way vindicated for mass use as a nootropic.
The following is extracted from research I did for a client (which I’m sharing with their permission). An important thing to keep in mind while reading this is that the information was gathered to answer particular questions (Primarily “quarantine procedures for very risk sensitive, cost insensitive people”), and that biases what I looked at in weird ways. But I think it’s still much more useful for some set of you to have this information than not, so here it is.
Of young, healthy people caught by prophylactic screening (typically contact tracing), 30-50% who test PCR+ will never report symptoms (in some cases these subjects are proactively screened for temperature, in others it’s not clear. Additionally, other studies have found that some percentage of people who report no symptoms will go on to develop CT lung anomalies). Additionally, most people who do develop symptoms spend several days being contagious before they develop symptoms. So symptoms are not a very good metric at all for determining if someone is infectious.
PCR tests look for specific viral RNA sequences and amplify them to make them easier to detect. They can vary in a number of ways:
Specific sequence searched for
Number of amplifications done
Collection site and mechanism of sample
PCR false positives are quite rare, and typically have to do with sample contamination. False negatives are more common, and can come from a variety of sources:
Covid was present but did not have the particular sequence searched for
Did not do enough amplifications to notice effect
Patient has covid but the particular site sampled does not.
How common are false negatives? That’s hard to define, because currently a nasopharyngeal PCR is what gets you diagnosed as having covid- if you fail that, you’re assumed to have one of the many things that produces similar symptoms. However, we can make some guesses.
The following graphs show the calculated chance of testing PCR+ on a nasopharyngeal test on a given day after exposure, given frequent testing and an eventual positive result.
But that’s just for nasopharyngeal (NP) tests. Data on sicker patients (the only ones studied) show it’s possible to have a negative NP test while another area of the body (lower respiratory or gut) tests positive.
But these are all people who tested PCR positive eventually. What about people who get sick without ever testing positive? A very small study found that of 24 health care workers who developed positive antibodies over a 3 month period, 10 never had a positive PCR test despite being tested twice weekly. The paper offers multiple explanations for this, and I’m very reluctant to draw conclusions from such a small study, but it is concerning.
Antibody tests look for an immune reaction to viral proteins. They can be negative when a person is contagious (because they haven’t formed a large enough reaction yet) and positive when they are not (because they successfully fought off an infection).
A reasonable question I have not investigated is “does an antibody+ test mean I’m immune?”
Like PCR, LAMP tests look for specific viral RNA sequences and amplify them to make them easier to detect. LAMP tests go through many fewer amplification cycles, making them less sensitive but much faster: 30 minutes vs 2-3 days for PCR, plus the transit time for the PCR samples.
A LAMP test every three days is much more valuable than one PCR test, because catching the peak is much more important than the sensitivity. I’m not sure if a LAMP test taken today is more or less useful than a PCR test taken to give results today. I stopped digging into this because there were not yet any LAMP tests on the home market.
Antigen tests look for specific viral proteins in a sample. There’s no amplification, which makes them less sensitive, but manufacturers report catching 88% of cases caught by PCR, so maybe this is fine, especially since you get results days faster?
The 88% sensitivity number is much, much higher than you see in literature (which is something like 20%-50%), I assume because they used more abundant samples. There’s some controversy over whether that’s because many PCR positives are driven by dead virus, in which case the antigen test returning a negative result is a feature, not a bug. This may well be true, however at least one study was able to culture live virus from a PCR+/antigen- sample, so it’s not foolproof.
Of the studies looking at antigen tests, all that I found either started post-symptoms, or took a random sample of people showing up at a sampling site. None were in a position to determine how good antigen tests are as an alarm system for catching an early infection (as opposed to diagnosing symptoms or determining when someone has ceased being contagious)
However antigen tests return results in minutes, while PCR tests take 2-3 days to complete not including shipping time. Given how quickly covid multiplies, it’s possible that an antigen test now is more sensitive than a PCR test from four days ago, especially if the exposure occurred in the intervening time.
That’s a good question, which with the exception of asymptomatic spread can’t really be answered without human challenge trials, which the entire world declined to do. I would be surprised if any of these tests’ thresholds lined up perfectly with the threshold of infectiousness, because there’s no reason to expect they would. I expect culture tests to be much closer, but still not necessarily exactly on line (plus AFAIK they’re not available for diagnostics, even through a doctor). Given that I asked…
How long do I need to stay in quarantine after potential exposure?
The best data on this is from New Zealand, which has a very strict isolation policy for entrants: 14 days isolation, with PCR tests on days 3 and 12 of isolation (a pre-departure test is required only if you’re coming from the US or the UK). By my earlier estimations, day 3 of isolation is already likely to be past the peak of detectability, unless travellers were exposed right before they left. Nonetheless, New Zealand reports only a handful of import-related covid cases after this policy kicked in, and a model attributes those to people who caught covid in isolation (e.g., a couple who shares a hotel room and one partner gives it to other on day 4), rather than people who entered New Zealand infected.
I did look for similar data from other countries, but NZ had both the best quarantine and the best data.
So despite the tests’ low sensitivity, 14 days + a test at the end really does seem to be a long-enough isolation period.
For those of you just tuning in: on a genetic level, all parental investments in their offspring are equally valuable. From the offspring’s perspective investing in them is two to four times as good as investing in their sibling (depending on if they’re half or full siblings). The fight to get the amount of resources they think they deserve is parent-offspring conflict
One manifestation of parent offspring conflict is weaning conflict, where offspring would like to keep getting nutrients with no effort and their mom would really like them to go out and get a job.
But it can start before then. Conflict over exactly how much nutrition a fetus should get may contribute to preeclampsia (high blood pressure during pregnancy) and insulin resistance (PDF). This is not just about mothers not wanting to give up nutrients- more nutrition leads to larger babies, which is almost always good for the baby but kind of hard on the person forcing it out through their vagina. There is even speculation that the human custom of making a thick uterine lining (nutritionally expensive) only to flush it away each month evolved as self defense against a placenta that would otherwise invade your uterus like ivy invades bricks.
Creepy, yes. Abhorrent, at the level of individuals. But totally logical and predictable from the level of a gene.
The typical explanation for motion sickness is that your inner ear and your eyes disagree about whether or not you are moving, your body interprets it as food poisoning, and prepares to throw up. This does not quite make sense to me, because it fails to explain any of the following:
Why being a passenger is so much worse than being the driver.
Why playing video games (eyes say movement, ears say stationary), reading in a bus (eyes say stationary, ears say moving) and riding a roller coaster (eyes and ears both say moving very fast) produce the same feeling.
Why smooth rides (subways, no-turbulence airplanes) are so much easier than busses, or why highways are easier than stop and go traffic.
Apparently other people consider nausea a stomach issue, but for me it’s very much a head issue. Motion sickness also gives me headaches. What’s up with that? Why is it so tightly correlated with sinus pressure?
Why does low blood sugar feel so much like motion sickness?
I’ve never experienced this, but television assures me heavy drinking produces the same effect. Why?
Why does motion sickness give me temperature fluctuations.
I’ve heard a partial explanation for #3, which is that your inner ear actually senses acceleration, not movement, so a steady velocity doesn’t feel like movement. And we have a very compelling proximal explanation for #6: the difference in density between water and alcohol stimulates your inner ear both as you get drunk and as you sober up. So obviously the inner ear is very involved in this, but how?
Alternate hypothesis: motion sickness is designed to keep you from eating, because your body is not in a good state to digest. One way that can happen is if your sympathetic nervous system (responsible for fight-or-flight-or-stand-there-being-really-anxious) has kicked in, because it redirects blood flow and energy to things that are immediately useful in escaping from tigers (muscles, senses) and away from things that solve future you problems like digestion and the immune system (which are regulated by the parasympathetic nervous system).
Both the sympathetic and parasympathetic systems are regulated by the hypothalamus. For fun I googled “hypothalamus motion sickness” and the first result was this rat based study,* which put rats in a “animal centrifuge” to induce motion sickness. I couldn’t find video of a rat centrifuge, but NASA helpfully provided video of a dog centrifuge. It looks not quite as bad as a tilt a whirl, although the rats were exposed to double gravity so I should probably cut them some slack.
During their amusement park adventures, the rats experienced a spike in histamine production in the hypothalamus (how cool is it that we can continuously measure that?), and caused the rats to display characteristic motion sick rat behavior. Inhibiting histamine production or removing the inner ear (the part that detects motion) caused both of these to disappear. Histamines also help regulate body temperature, so that’s #7. This suggests that anti-histamines would be useful at fighting motion sickness. The good news is that this is correct, the bad news is that they make you sleepy and possibly give you Alzheimer’s. That’s fine for any one time but I don’t want to make a lifestyle out of taking them.
A website my laptop unfortunately ate the link to has a subtly different explanation: your brain tracks motor movement via an efference copy, creates a prediction of what sensory changes that should create, and they compares that to the actual sensory input. Motion sickness might be your brain saying “these are too different, abort, abort”, or buckling from the intensity of calculation needed to reconcile the input.
I have always wondered why I/people hold my (our) breath during times of stress. Unless you’re being hunted by a xenomorph right that second, oxygen deprivation is not helpful.
The most convincing hypothesis I’ve found is that your brain can only do so many calculations per second, compensating for breathing takes calculation, so you stop breathing. That this rapidly starves your brain of oxygen, lowering the number of calculations you can do, is exactly the kind of long term thinking I expect from the human body which, lest we forget, takes in air and food through the same hole. If both breath-holding and nausea can be caused calculation overload, we would expect the same things to cause them both. I can think of two things that do exactly this off the top of my head- sparring (but not drills) in martial arts, and playing Katamari, both of which involve complex spatial reasoning. These are not great examples because there’s a lot of confounding variables, like extreme physical exertion while being hit in the stomach.
To summarize my speculation: sensory input requiring too high a rate of calculation points you towards your sympathetic nervous system, which makes you nauseous so you won’t eat while you’re not capable of digesting.
This suggests that anything that kicks you towards the parasympathetic system should reduce motion sickness. Unfortunately the parasympathetic and sympathetic systems run on the same neurotransmitters, so looking at the relevant drugs does not provide useful information.
This also suggests that anything that lowers the number of calculations you need to do will be helpful. BCMC tested a heads up display that showed users their head position relative to the horizon.
Studies found it overwhelmingly helpful, although I haven’t dug into that paper in detail yet. Unfortunately there’s no way to purchase the technology, so I’m left hoping someone picks up the patent.
In conclusion: we don’t really know what causes motion sickness and that there’s no known really good treatmen. I am going to experiment with consciously tracking my head position relative to horizon and with rhythm games (which help integrate sensory data).
*The second result appears to be the exact same experiment, done 10 years earlier, with the exact same result. It’s nice to see something reproducible.
I’m taking on sinus inflammation because it’s a major contributor to my motion sickness, which is a major contributor to making commuting suck, and commuting is one of very few things that can actually depress your hedonic set point (psychologist talk for “make you miserable”). My doctor has suggested xylitol nasal spray, which she claims inhibits irritation in the sinus cavities. Quick googleing reveals it’s also considered useful for bacterial plagues on the teeth and in the arteries. Let’s dig in.
Xylitol’s main claim to fame is as a calorie-less sweetener in humans. The claim is that it kills (many but not all strains of) bacteria via the same mechanism: it can’t be converted into energy, so the bacteria starve to death. This has to be to be missing a step. Bacteria are surrounded by billions of molecules they can’t digest all the time, and they survive that. If xylitol is to have an affect it must not only be indigestible, but inhibit digestion of actual sugar. Off the top of my head there’s two ways that could happen. In the human body, sugar is moved around by the blood. If xylitol takes a sucrose molecule’s ticket to a particular area, there will be less sugar there for bacteria to eat. The downside of this is that you might starve out your own cells. Another option is that bacteria cells themselves become confused by xylitol. The ideal would be if xylitol fit into a sugar receptor but couldn’t be taken into the cell, so the receptor was blocked indefinitely. Or if it was taken in it could trigger a “yup, we got a sugar” reaction that caused the cell to take in sugar later, but I’m not sure why a bacteria would ever turn down calories.
I found a lot of studies on xylitol and dental use. Most of what I learned is that dental abstracts are more like teasers than summaries, not cluttering up the space with numbers or sometimes even conclusions. Overall there seems to be a mild consensus for xylitol mildly inhibiting cavities, although it’s certainly not a substitute for fluoride. Also I totally should have been chewing xylitol while I was recovering from surgery, since is almost certainly disrupts oral plaques, although I worry about what it would do to the intestinal biome.
What about sinuses? I found a lot of very small studies, but 5 studies of size n are not equivalent to one study of size 5n. You don’t know how many more studies of size n were done but not published.
This study and this one found decreases in medical severity (as measured by the SNOT-20 score. Yes that’s it’s real name), but not self-reported pain (as measured by the less well named VAS score). This study in rabbits was well controlled (if small) and found significant decreases in bacteria.
This study found that a nasal decongestant spray worked better than xylitol or saline spray, which worked about equally as well. Nontheless it’s conclusion was that [name brand of xylitol spray] was an effective treatment for nasal congestion. It also spelled spray with an ‘e’ . Twice.
One interpretation of these results is xylitol helps impedes infection but irritates the sinuses such that there’s no change in pain levels. Another is that people are really good at suppressing conscious knowledge of pain. My experience has been I’m really good at suppressing moment-to-moment awareness of pain but I do notice when asked (which is how I went weeks without treating my dental neuralgia, and then suddenly noticed I was at 8 on the pain scale), and that the pain has a great deal of effect on my behavior and happiness whether I acknowledge it or not. And if I keep using xylitol I need to change my brand to one that, when it buys positive press in a supposedly objective forum, spells its own name correctly.
Left untreated, people with phenylketonuria (PKU) can develop intellectual disabilities, seizures, and “other medical problems”. But PKU does not cause any of those. Phenylketonuria + a normal diet causes a build of of phenylalinine in the body, which causes those problems. If PKU is caught at birth and the sufferer is kept on a phenylanlinine-light diet, they will never develop these problems.
Henry Markram suggests that something analogous is going on with autism. He and his collaborators think that the actual problem is that autistic babies have extraordinary sensory sensitivity, and this sensitivity causes defenses that cause them to miss certain critical information during developmental periods. What is challenging but achievable (the zone necessary for learning) for other people is overwhelming for them, so they don’t learn. The developmental window closes and they’ve lost their chance to truly master that skill. But if they were given stimulus in their zone of achievable challenge, they would learn those skills and maintain them for life. They might continue to need accommodations, the way phenylketonurics need to stay on a phenylalinine-light diet their whole life, but with those accommodations they could function “normally”. This is known as the intense world hypothesis.
The example they give is the critical period for learning language. You *can* learn a new language after the critical period, but it will never be as easy, most people will never attain genuine fluency, and if you never learn any language it may be truly impossible to pick one up later. If normal human speech is overwhelming to an autistic infant they will miss that period and their language will be impaired for life. But if they’re given regular access to speech they are comfortable with (probably quieter and slower) they could learn it just fine, the same way hearing impaired children do fine with sign language.
I was also really impressed with the writing of this lay-press article. I’ve been avoiding doing take downs, especially of popsci articles, because there are millions of wrong things every day and criticizing them is easy. For a while I could justify them as case studies in critical reading, but now it just feels bad. This had led to a lot of aborted blog entries, as I read something amazing and then realize it’s too flawed to pass on uncritically. I don’t agree with everything the article says (insisting there’s only one cause of autism strikes me less as brave and more as idiotic), but it lays out its case in an informative and responsible manner.
The biological/scientific definitions of heredity and heritable differ slightly from the popular usage. Lay people tend use it to mean “how much is this caused by genes?” In science, heredity is how closely people resemble their parents, divided by the total variation in the population. Biological sex has almost zero heritability because knowing someone’s parents sex does not allow you to predict their own sex.* Number of arms is barely heritable, because there’s almost no variation in number of arms among humans, and what variation exists is overwhelmingly caused by environment, not genetics.
A corollary to this is that a measure of heredity is only valid for the exact environment you measured it in. If you plant a variety of seeds in identical pots and give them identical water and supplements, most variation will be due to genetics, and a small amount to chance (which will be counted as environment), so traits like height and time to flower will be highly heritable. If you plant those same seeds in widely varying pots and vary the water and nutrients they get, a lot of the variation will be due to environment, and the heredity values of the same traits will be much lower. Skin color in Norway is more heritable in the winter than in the summer, because teenagers deliberately tan more than their parents.
I have struggled before to make effectiveness estimates when the intervention’s usefulness depends on multiple factors. Blood for car accident victims is only helpful in the context of emergency rooms and medical schools and sterile gauze. Suicide hotlines require phones and electricity and suicidal people at a bare minimum, and active rescues require police and mental hospitals and often pharmaceutical research. I think I’m just going to have to put effectiveness in the same category as heredity: the quantification is only valid for the environment in which it is measured.
I’ve worried before about Effective Altruism’s tendency to take the existing system as a given. That was a reasonable simplification when the movement was first starting, and there was plenty of low hanging fruit that didn’t require more sophisticated analysis. But I’m really happy to see organizations like the Open Philanthropy Project branch into studying how to change systems and how to measure the effectiveness of attempts to do so.
*Intersexuality confounds this a little but my impression is it’s mostly not a genetic issue, in part because intersex people generally have difficulty reproducing.
Barack Obama recently announced doubling funding to fight antibiotic resistance, which would be more impressive if there wasn’t a significant step that cost the government nothing: ban use of antibiotics for livestock, which currently account for 80% of antibiotics produced. Hell, taxing use of antibiotics in livestock would reduce the problem and generate revenue. Representative Louise Slaughter has introduced a bill to (more or less) do this for five years running and it has gone absolutely no where. So this feels a little like California introducing water restrictions on people while saying nothing about agricultural use, which coincidentally is 80% of their water use.
But maybe Obama’s new money will go to one of the lesser contributors towards antibiotic resistance: people who don’t finish their prescriptions. Researchers are studying a new microchip that sends a signal when it is being digested. They’re using it for severely mentally ill patients, who for various reasons sometimes have trouble staying on their meds (good luck to the first schizophrenic to explain to their new doctor that their old doctor tracked their medication by making them swallow computer chips), but what if we used them for antibiotics?
This isn’t a simple solution. To have it do any good you have to either punish people for not finishing them (which is extremely hard on low income people) or pay them for finishing (hello terrible incentives). People who split prescriptions are often trying to save themselves the doctor’s visit more than the cost of the medication itself, and this doesn’t address that. But it seems like we ought to be able to do something with this.
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.
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.
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
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.
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.
A 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.