8. Patrick Finan, PhD: The Interplay Between Pain and Sleep

Hello everyone, I'm Dr. Darsha Shah, and I'm Dr. Altamash Raja, and welcome to Medicine Redefined, a podcast where we will explore the often overlooked but necessary components of health, what we consider to be the fundamentals. We will investigate topics and practices that can give you and your patients the best chance to optimize a healthy lifestyle. It's time to move the needle forward and put the health back in health care. Before we get into the show, here's a quick message from Physician Financial Services. A business widely recognized in the Physician Community for Disability Insurance, Lawrence B. Keller CFP has been in the Insurance and Financial Services Industries since 1990. Unlike medicine, which has a standardized path that physicians must take to gain the education, training, and experience requirements necessary to obtain board certification, the Insurance and Financial Services Industries does not. While he might not be a doctor's first phone call regarding their insurance needs, he is often their last. Find Larry at Dr.Podcastnetwork.com for slash Larry Keller, or at the link in the description of this show. Alright, hello everyone, welcome back to another episode of Medicine Redefined. In this episode, we get nerdy with Dr. Patrick Feinen, who is an associate professor of psychiatry and behavioral sciences at Johns Hopkins University. His research includes the understanding of the relationship between sleep and pain. And we really try to break down each category on its own first, pain, and then we go into sleep. And then Dr. Feinen does an incredible job tying the two together. This is really a fascinating topic where the research has only touched the tip of the iceberg. Alright, let's flood your brain with some knowledge. Alright, Patrick, welcome to the show, man. Hey, thanks, thanks for having me. You know, Patrick, it's funny, I think that we met, I guess, some time around 18 months ago. And the way I came to learn about your work is basically one of those little recruitment flyer things outside of the medical school bathroom, where it's like, grab a tab and learn about this study. And we met up in your lab and I kind of got to learn a little bit about your work and two topics that we're going to discuss today that we have, what I think is extremely poor understanding when it comes to medicine, and especially in medical school, we don't learn a lot about it. So I'm definitely excited and you were kind enough to kind of get me on to this project, but unfortunately, then the world stopped and we haven't really made much progress on that. So I've been stoked about this conversation and I'm so excited to learn, man. But for our listeners who might not know who you are and don't know much about your work, why don't you tell us a little bit about your journey, how you got to where you are now and what it is that you do. Sure. I'm going to have to compliment my research team on the recruitment tactics. They're able to snag you from one of those pull tabs. That's good work. We need to do more of that. And yeah, we've been shut down, like everybody else, but we're getting back up. So yeah, I'm an associate professor in the Department of Psychiatry and hang on one second. I'm sorry. I'm getting some feedback here. Okay. I'm an associate professor in the Department of Psychiatry at Johns Hopkins. And my work is really broadly focused on chronic pain mechanisms that contribute to adaptation to chronic pain, vulnerability to chronic pain and resilience over time. So we try to approach pain from a kind of whole, I would say a whole holistic angle, a whole person angle. And that's kind of how I got into sleep through being really interested in the mechanisms. And what we found out over the years is that when we look at how people with chronic pain sleep on a day-to-day basis, it kind of unlocks a lot of insights into their kind of day-to-day function. It's super fascinating. So I mean, this conversation is going to be about pain and sleep and something that a lot of people I think don't really connect together. But let's first separate the two if we can. Talking about pain, it's obviously a very complex process that I think a lot of humans probably don't understand. I mean, when I think of pain early on, I'm thinking something that I'm touching and I wish maybe a sensory nerve signals my brain and then there's some feedback loop. So can you kind of just break down what is pain? Are there different types of pain? How should we think about it? Yeah, good question. So definitely there are different types of pain. I think the best way to kind of break it down is the classic conceptualization of pain from the early Melzac study. So if we think of pain as having three core components, there's a sensory discriminative component and that is the aspect of pain in which we are able to kind of determine, is this stimulus painful or is it just warm? Is it painful or is it cold? So that's the sensory discriminative component. There's a cognitive evaluative component and that's the piece of pain where we kind of make decisions around what to do when we experience pain. And so that, of course, interacts with the sensory discriminative component but has its own kind of set of decision-making parameters and different parts of the brain that are responsible for driving those types of thoughts. And then finally, there's the affect of motivational component, again, interrelated with the other two, but that part of pain typically is characterized by the kind of emotional state that one is in when you experience a painful stimulus. And those emotional states are going to drive decisions, they're going to stamp in memories and so it's really kind of all three of those components are interlocked and it's important to be thinking about all of them. Yeah, that's pretty fascinating. It's definitely more in depth than what we have learned about in pain. And I think that for those of sometimes people misrepresent like what we do, we're physical medicine rehab. Sometimes people will say pain medicine rehab just by the sheer volume of how many people we see and pain such a universal thing, right? Every single person who's listening to this has experienced pain to some degree, they are definitely not thinking it from the lens that you just described it. But, you know, touching on to your last point about the emotional component. This past year has been, I mean, I guess we're up about in a year of lockdown at this point and, you know, it's been high anxiety, the emotions have been kind of up and down for very different reasons, right? Are you familiar with these or any literature coming out now that's talking about the prevalence has gone up because of that, because of the changes in emotion? That's a good question. I can't say that I've read anything that's kind of linked it specifically to that. I think we can expect that to happen. We are seeing that rates of pain are increasing. We know, for example, that COVID-19 is related to just like a number of viruses are related to increases in pain sensitivity. The case of the long COVID, which is kind of increasing in how much the public is becoming aware of it, is really starting to look like a lot of the chronic pain syndromes that we see. You know, if you take a look at things like Gulf War syndrome, these types of chronic pain syndromes that come about through sort of mysterious potentially viral sources and also traumatic sources, everything's kind of aligning in that way. So we're seeing those types of pain increase. Of course, then you can extrapolate from the mental health data that's coming out where we're definitely seeing dramatic rise in depression that we would then expect to see increases in chronic pain result from that, because that literature is really well-founded. We know that when we see increases in depression, we're going to also see increases in chronic pain sort of lag right there. So yeah, Patrick, I think that makes tremendous amount of sense. There's been a lot of talk lately and from the literature that I've been looking at, we're familiar with no repinephrine and serotonin and their integral role that they play in both mental health and obviously chronic pain and how they're correlated with each other. But the dopamine signaling pathway is somewhat of a novel idea. So what are your thoughts on this and what does a literature tell us about its role in pain specifically? Sure. So we know a few things about dopamine. We know dopamine produces endogenous analgesia. It's recruited in the face of various no-susceptive insults. We've seen this in pre-clinical literature. And then in the early 2000s, there started to be a series of studies that started to demonstrate this in humans. In a few studies with patients with fibromyalgia, we've seen differences between cases and controls in dopamine binding using pet methodology. We've seen differences in dopamine metabolites in the CSF of patients with fibromyalgia compared to controls. And then in addition, we've seen a few candidate gene studies, sort of early candidate gene studies, suggesting that there were differences in rates of the expression of the comp gene, the catacole and methyl transferase gene, which regulates dopamine signaling. So that kind of formed the basis of a lot of interest of pain researchers to try to figure out what might be going on with dopamine. And for me and some of my colleagues, we've kind of taken that to suggest a couple of things. One, we've hypothesized that if there are dopamine-nergic differences in patients with chronic pain, then we would expect to observe behavioral and emotional differences that would reflect that kind of alteration in dopamine-nergic signaling. What types of behavioral and emotional differences would we expect? One, we would expect there to be differences in the ways in which patients with chronic pain experience rewarding activities. We would expect there to be differences in the degree to which patients with chronic pain are able to experience positive emotions. And possibly the degree to which positive emotions are able to sort of serve their function in patients with chronic pain, either by being sort of analgesic agents. So the expression of positive emotions has been robustly demonstrated in the literature to be associated with analgesia. And so we would expect there to be differences there. And possibly we might expect there to be differences in the way in which patients with chronic pain experience drugs of abuse. And some of these questions have started to become answered. We've seen in the last several years a number of studies showing that patients with chronic pain indeed seem to evidence reward processing deficits. We've seen this using experimental tasks. And in my lab, we've observed not only deficits in reward processing to natural rewards, you know, rewards like money. But we've also seen differences in the day-to-day experience of positive emotions. And that's kind of where our focus is in trying to really narrow in on how can we develop treatments that kind of stem from this possible reward deficit that we're seeing in patients with chronic pain? Yeah, I mean, that's truly fascinating stuff. I think I probably should have started with this. I think it's worth taking a step back and just explaining exactly what dopamine is. I mean, you know, for those who don't know, we have a bunch of neurotransmitters, right? Some of the common ones that people probably are familiar with is serotoninist, the one that, you know, makes you feel good, you know, we have GABA, we have acetylcholine, norepinephrine, which is kind of like the adrenaline, your body's endogenous opioids, which you talked about. So dopamine is the one that's implicated in that reward pathway. You've talked about that already. But it's the one that kind of has the addictive properties, you know, exercise will increase your dopamine levels. That's kind of part of the reason why you feel good afterwards. Food has a tremendous thing. You know, when you take that ethepizza, you know, you get this massive dopamine response. And of course, drugs like cocaine and stuff. So I think that that probably people can probably have a better understanding of what that is. But I want to go back to this point about the comp gene that you had talked about. See a little bit more about that because one of the things that Darshan and I are fascinated about is, you know, this idea of precision medicine. And I think that more and more people are starting to learn, you know, go through their 23 and me or ancestor DNA and learn about these snips, right? The single nucleotide polymorphisms. And we know that something like the APOE is implicated with Alzheimer's and cardiovascular disease. You know, previously Dr. Arnold was here. He talked about the act one gene, which is more for like power athletes. And the science isn't quite there yet. And I imagine with comp, it's probably similar, but you know, it sounds like it's exciting stuff. But what does it tell you? What does it tell us in science in terms of, you know, how different people might perceive pain because that's an important thing? Yeah. Well, so yeah, I think you have it right. I think the comp studies largely came about in the early days when folks started to realize that they could measure these things called snips, single nucleotide polymorphisms and get data sets that, you know, allow them to use this as like an individual difference factor. So a snip can tell us a little bit about something. It can tell us, for example, whether a part of a gene is likely to have a function at a molecular level. But then there are so many kind of intervening variables that can kind of muck that up. And the early snip studies, comp included, were largely run in samples that were far too small to really have the power to be able to detect kind of meaningful differences. And my dissertation was a good example of that. So I did a dissertation looking at comped Val 158 met snip differences in patients with fibromyalgia. And we were looking at the degree to which having a quote-unquote risk allele on the Val 158 met snip was associated with differences in positive emotional functioning from day-to-day. So you can, that genetic work is important because it generated a lot of ideas. And they're very well maybe a realistic signal in those data. With respect to the comp gene and pain, I think the field has kind of largely moved on from the idea that we can reliably use an allele that someone may or may not have to accurately predict whether they're going to have pain, for example, or whether they're going to develop a mood disorder in the course of their illness. The data just never materialized to kind of achieve that hope. I think large-scale genome-wide studies have since taken over and that works ongoing. So something at a massive scale may one day demonstrate some kind of predictive utility there. For me, that work really was just pivotal in trying to think through a couple of things. One, it helped me think through what measuring something like the comp gene and the Val 158 met snip couldn't do. And what it couldn't do is tell me whether there was actual, for example, dopaminergic changes going on on a day-to-day basis. I could presume that somebody might be predisposed to have an attenuated dopaminergic response to a physiological insult. But that's always just going to be an assumption, right? You're assuming that because of the kind of presumed molecular action that that might be the case. But what you can do is then start to generate hypotheses from those signals and take a look with methods that are maybe more reliable, more robust, things that you can more accurately measure in kind of smaller samples that are feasibly accomplished in human subjects research. And that's kind of what we've tried to do. So we're doing studies where we're really trying to understand reward processes broadly in patients with chronic pain. And that's frankly how I got into doing sleep research. We talked about sleep earlier on. And what we realized kind of about a decade ago is that a lot of the reward-related mechanisms that we were interested in chronic pain appeared to be modulated by sleep. And there was this kind of bubbling literature demonstrating that sleep was robustly associated with pain. And so one of our core hypotheses that we've been tracking down in a number of different ways over the years is that this association between sleep and pain may be driven to some extent by deficits in reward processing, deficits perhaps in dopaminergic functioning, deficits building up from dopamine deficits in corticosterietal function that might be important to try to track down. So that's what we've been up to. Yeah, that's a pretty awesome explanation. Do you know if that comp gene is like with 23 in me or these online DNA things that self DNA kits that people can get if they give you that information, whether you have that gene or not? Because I hadn't heard of that until I read your work. That's a good question. I don't know if that's like available in commercial assays. It's a super common. Is it? Okay. Yeah. Yeah. It's one of those, you know, if you look up Val 158 Met Snip, you'll see, you know, just about every complex behavioral trait associated with it in one way or another. Okay. I see. Yeah. Yeah. I know. I got to go back and look at some of the raw data and stuff to see if that offers it because you know, my fear is, so what you were talking about before, this is the classic thing, you know, genotypic versus phenotypic expression. And right, and this is why the science of epigenetics is so fascinating is because obviously we know so many things after the genes that you've been encoded with like your environment and, you know, the way that your behavior and stuff will influence and in pain as complex as it is as you've described it is, you know, affected more so than almost anything else. And I know that there's literature out there like when we're talking about doing procedures on people, by just by simply telling them, hey, that like, you know, when you're giving them anesthetic like lighter can, but simply telling the patient that this is going to pinch or this is going to burn, the perception is that that procedure is much more uncomfortable rather if you, you know, as opposed to if you didn't tell. So, you know, if somebody was to see this data for themselves and you touched on how they might be likely to develop in the future, you know, I just seems like a scary proposition to kind of give that data, but yeah, I don't know if it's even available or not. But I want to go back to, you mentioned a couple of times that in terms of this specific genes and then the dopamine signaling pathway, you were looking in fibromyalgia, right? That's part of what your research was on. Do you know if other, you know, pain states like RA or inflammatory conditions like that or just like, you know, mechanical pain, if they have a similar mechanism or is the dopamine signaling pathway implicated in that or is it primarily just fibromyalgia that you guys have looked at? No, I mean, fibromyalgia was, that was like some of the early, the early literature. There have been reward processing deficits and I believe also dopaminergic deficits, although I'd have to go back and check my sources, but certainly broadly reward processing deficits observed in a variety of chronic pain conditions. I think, I think the reason folks started with FM is because the constellation of symptoms in FM really kind of dovetailed nicely with the proposed theoretical mechanism by which dopamine may alter function, right? So with fibromyalgia, the constellation that you very often see is sleep deficits, the experience of depression and anxiety and then widespread pain, right? It's like those three and you rarely see just kind of pain alone. And so I think, you know, dopamine is a neurotransmitter that serves a variety of other neurotransmitters, right? It's not an endpoint. It's more like a messenger in between. And so you would expect there to be kind of a wide net cast. And so I think that's why the early studies focused on fibromyalgia. You know, Patrick, as a, as a doctor on the wards, I'm seeing mental health issues every single day, right? From bipolar to schizophrenia to depression, fibromyalgia. And I'm very interested in the kind of this chicken or egg situation. Is it, is there any research that shows that it's the pain that's causing these mental health issues or is it usually the mental health and then the pain's coming along with it for the ride? Is there any research that kind of shows one or the other? Yeah, there's no definitive research that kind of points to one direction. There's lots of research showing that each of those conditions can lead to the other and that they're highly comorbid with one another. And, and so there is a sort of, when somebody develops chronic pain, I think it's a reasonable assumption that if there's not a history of mood disorder on board that in developing a pain treatment plan, it would be a good idea to kind of keep an antenna out for that type of problem to develop over time. To, to think about the, the possibility that repeatedly dealing with pain on a day to day basis, the loss of function, the loss of social context that often occurs really is like a breeding ground for the development of a mood disorder. And, and having that kind of foresight early on in a pain treatment plan, I think would really go a long way to helping patients ward off those, those types of. So I wanted, I wanted to follow up on this. So I read a, I read a book called the Anatomy of Hope by Jerome Grootman. And he's, he's a famous like doctor writer. So he talks about how he dealt with back pain and he ends up going to like Beth, Israel and Boston. And he meets this famous doctor. I can't remember the name, but essentially the doctor's telling him, Hey, a lot of your pain is just mental. It's, it's, it's these patterns that you're forming, the trauma, tightening your back, all these things. So from your standpoint, you know, is it worth us providers going to the medication first to treat the pain and hopefully alleviating some of those symptoms? Or would you rather take more of a mental health approach to these, you know, neural patterns that patients might be forming with their pain? So, you know, it's tricky. I think the first thing we can take a step back and there is an interesting kind of discourse in the research world, in the clinical world around this concept that pain is, is quote, unquote, mental, right? So to phrase it in that way can be really stigmatizing for patients. And patients will almost uniformly recoil at that kind of phrasing, right? The idea that it's all in all in my head, that's like the one that you're most, right? And, and what, what, as, so I'm a pain psychologist. And as a pain psychologist, the first thing that I have always done working with chronic pain patients is kind of address the elephant in the room right away. And that elephant in the room to me is, is, all right, let's, let's talk a little bit about the neuroscience of pain. We know that pain is processed in the brain. And that, that is just when you experience pain, it's because your brain's working in a way to communicate signals that let you know that you're in pain. So that's a good thing. So we are, we're going to accept right now that pain is in your head. But we're going to refute the notion that it's all in your head, quote unquote, right? And, and we're going to, we're going to sort of just radically disavow this idea that any patient with pain is kind of making up their, their symptoms or experiencing their symptoms as some kind of secondary reaction to an emotional trauma. So we, we, I think that is, is a really important place to start to kind of let patients know, all right, your, your brain, your emotions, your thoughts are all critical to how you experience pain. And maybe critical to your recovery from pain. But that doesn't mean that, that any of us in the room think that you're making these up or you're looking for something else other than just to try to feel better. So that's kind of like an, an important issue that as a pain psychologist, I find, I've found myself having to deal with right away because patients will often be really on guard. And, and in many cases, resistant to engaging in the type of pain self-management practices that require an acceptance of the fact that the way we think might influence, for better or worse, the degree of pain that we're experiencing, that our emotional reaction to experiencing a spike in pain may facilitate further pain. And if we can work on control, we may not be able to control the degree of pain that we're experiencing depending on what's going on, right? We might not be able to control that, but we might have a good chance of controlling the types of thoughts that pop up associated with those pain insults. We might have a good chance of controlling the types of emotions that are associated with it. And, and, and that can sort of bring the power back to the patient and help them on their journey. Yeah, you know what's interesting is I don't know exactly when we started. I think that at least at our institution and a lot of the smarter physicians who that I've learned from who are doing pain management, they started to appreciate the biopsychosocial model a lot more, right? We know that as a staple of treatment for somebody who's in chronic pain, CBT is part of it. It's a multi-disciplinary approach, even though there if there's a, you know, a biomechanical issue that's wrong, you're going to try to address that, but that's not going to cause a hundred percent resolution. So they have to, you know, try to, you know, tackle it from multiple different approaches. And, and I think that's something that's really important to understand. It also falls on us as providers to to be very selective with our words, because at the end of the day, you know, as I alluded to earlier, like, you know, they're powerful and just by telling somebody, hey, that this is going to hurt, like that can cause it to be much more unpleasant experience. And so somebody who's already hypersensitive and they're in this hypersensitive state, it's going to make it that much worse. There's an interesting book for you. I think that there's a, this PM&R doctor named John Sarno, he wrote this book called Healing Back Pain. Essentially, he talks about this concept of tension myocytis. I'm not sure if that's something you guys have heard, but essentially it's a very like psychosomatic approach to, you know, whether it's hamstring strains or, or back pain is kind of the most common thing that he talks about. But I want to pivot a little bit, though, Patrick, and ask about like just in states, like such as, you know, chronic regional pain syndrome or just anything, even fibromyalgia or something like that where you have this, this chronicity, you know, for, for longer, longer time. But then people have, you know, hyperelgesia or even aledinian for those who don't know, basically aledinia is, is, you know, when somebody, it's like some, a normal stimulus that shouldn't be uncomfortable causes extreme pain. So that would be if I was to kind of touch some, your arm, darsh, like, you know, you would have a tremendous amount of pain. So it should be non painful stimuli that evokes a painful potential, right? Essentially. So is, is there something unique when it comes to the mechanism, Patrick, about those specific instances, like those conditions? So you're asking about CRPS or you're asking about allergies in general. I think just like a hypersensitivity, because I mean, a lot of times with CRPS, you'll get aledinia, at least from what I've seen. But I, if you think they're different, I'd be here to, I'd be happy to hear the differences between them. No. So we can, we have some, some nice tools to be able to differentiate those responses in the lab. So we, we, we have experimental tools, part of a suite of things we call quantitative sensory testing that we can use to be able to tell whether there is a greater degree of, for example, hyperalgesia, sort of an exacerbation of pain to another wise painful stimulus, or aledinia, as you describe pain when the stimulus is not painful. The, you know, I think whether a treatment plan would differ depending on that, whether there's, for example, hyperalgesia or aledinia on board, I think is, that's going to vary on a case-to-case basis. From the biopsychosocial standpoint, we're going to take that information in, you know, each person's experience is going to determine how we're going to approach it across all levels in terms of what types of providers are you engaging with, right? You, you, you want to make sure that if a multidisciplinary care plan is necessary that you bring, you know, somebody on board. So if there's, for example, a clear kind of aledinic process going on, I might want to get a neurologist to, to check something out. Whereas if it's kind of purely musculoskeletal, there's not, there's, there's not a sort of clear neuropathic pain. Well, then, you know, that might change course and maybe we'll be thinking more about physical therapy. Or maybe we'll be thinking about all of these things. So yeah, we kind of take it on a case-by-case basis. I don't think there's like a clear rule of thumb that that will drive a comprehensive multidisciplinary pain treatment plan whether there's aledinia or hyperalgesia on board. Patrick, I'm extremely offended. You have two physiatrist sitting in front of you, but, you know, you get neurologists to shout out. What's that about that? Yeah, you're right. That was bad. Come on, man. It's a blatant problem. Well, Patrick, you mentioned earlier that your, your research now, you're starting to look into sleep a little bit more and it's association with pain. So I think this is just going to be a great segue now. As I got my blue blockers on, I feel my melatonin searching in my body. Can we talk about? Can you take us through sleep physiology? You know, just kind of the stages and the purpose of them. I think most people know about REM and maybe non-REM, but that's about it. I'm thinking. Sure. So those are blue blockers. I thought they were just cool-looking glasses. I'm impressed. You're anticipating the need to get to sleep after this at some point. Yeah. So you're asking just in general about kind of sleep physiology, basic overview. Yeah. So we tend to think about sleep in my world in kind of two broad dimensions. And there are other sleep folks who are going to get much more into the weeds on this than I will, but I'm going to give you the two kind of key areas. We think about sleep architecture. And so that's the sleep staging. And I'll walk you through that briefly. And then we think about sleep continuity. And so I'll start with sleep continuity. In sleep continuity measures, what we're looking at is the quantity of sleep that somebody's getting. They're total sleep time. We're looking at how long it takes them to fall asleep. We call that the sleep onset latency. We look at how many minutes they're awake in the middle of the night. We call that wake after sleep onset or wasso. We look at the total number of awakenings that they might have throughout a night. We look at their time of final awakening. And then behaviorally, we also look at the time that they got out of bed. Because in some cases, the final awakening might happen at 5 a.m. and they don't get out of bed until 7 or 8 a.m. And so that falls under the kind of broad rubric of sleep continuity, which the gold standard assessments are a sleep diary. So you just ask a patient to tell you the timing, the number of minutes, and the times in which they fell asleep and times in which they woke up. That used to be done with paper and pencil. Now there's a million apps that make it really easy for patients to input that type of data. And then of course, most people are familiar with all of the wearables that are out there that objectively track all of these things with typically with actigraphy, although there are other kind of ways to do this now. Actigraphy is basically looking at activity counts. So the most common way to do it is somebody wears an actigraph on their wrist. And when they fall asleep, typically there are very few movements. You got one on now, yes, like a Fitbit or really, you know, any of those wearable technologies have some kind of triaxial accelerometer baked in there. So we can get all those measurements really easily now. And that gives us a good sense of how much somebody is sleeping. The sleep architecture component is looking at the stages of sleep. So you know, we have the stages of sleep progress from sort of very light sleep to progressively deeper sleep. So the lightest sleep would be stage N1 and then you cycle into stage N2 sleep. We spend most of the night typically in stage N2. And then we spend about 20% of the night in stage N3, which is also known as slow wave sleep or the kind of deep sleep. And so there's a lot of interest in the degree to which one is able to achieve slow wave sleep. There are certain disorders and certain drugs that can make it very difficult to achieve slow waves and folks who have that phenomenon often report feeling that their sleep was very unrefreshing. So they may actually sleep a full night. They might get, if you look at their sleep continuity indices, you might see what otherwise looks like normal sleep. But if there's, for example, no slow wave sleep, that might contribute to the kind of experience of feeling unrefreshed in the morning. And then finally we have REM sleep. So the first three stage N1 and 2 and 3 are all N REM sleep stages. And then finally we have REM sleep. REM sleep also tends to happen about 25% of the night give or take. The predominance of REM is in the latter stage, the latter parts of the night. So you typically have more REM in the last kind of four hours of sleep and more slow wave sleep in the earlier parts of the night. Patrick, that's interesting. Yeah. So I was familiar with alcohol and its role is at just kind of curtailing REM sleep. I mean, I've read about that quite a bit and Matthew Walker speaks about that. And he's, I think most people probably know him from his book, Why We Sleep. But what specific drugs were you alluding to when you're talking about the N3 or slow wave sleep that you talked about? What kind of common medications might, you know? Opioids. Opioids is the number one that comes to mind. So opioids typically just knock out N3, slow wave sleep. Some people, it's not uniform, but it is, it's a very common phenomenon. And you can observe it really clearly in people with opioid use disorder who are on agonist maintenance medications. So you see, and we've published on this as well, really very little stage N3 sleep in folks with opioid use disorder. Wow. Well, this is the perfect segue because, like I said, you know, what kind of attracted me to your work is sleep is, if you've talked to me over the last two years, it's my favorite thing to do. I'm absolutely fascinated by it. And so, you know, my, the way that I wanted to look at, you know, basically pain was or sleep was as an antidote for pain essentially. And that's kind of what you've been working on for the last couple years. So it's, it's, it's crazy to me that when we're trying to address pain with opioids and, and you know, we know that sleep can have quite an impact when it comes to, you know, pain perception and sensitivity and how people, it just the whole experience of pain. So, um, talk a little bit about like what you've learned or what you're working on currently in terms of the relationship between sleep and pain. Again, is it a bidirectional thing? Is it more of a causal, you know, effect for it? How does sleep, you know, tie into just pain and the experience of pain? Yeah. So, like the question about mood disorders and pain, we see a reciprocal association with sleep and pain. So it's, it's not necessarily if we're, if we're trying to get to a chicken or the egg answer, there's not one that necessarily happens before the other. However, in the last decade, we've really seen a number of studies show now to the point where I'm pretty convinced that this is a real phenomenon that the, the bulk of the variance, the majority of the variance and the sleep pain relationship is accounted for by the sleep into pain directional pathway, more so than pain into sleep problems. And that might not be intuitive, you know, particularly folks who have chronic pain and, and will report very clearly, I couldn't sleep because I was in so much pain. It was what, you know, and so you, of course, are going to have lots of examples of people who will say, my pain inhibited my ability to sleep. And that's, that's absolutely a phenomenon. But if we look at the literature on the whole, including the experimental literature, the clinical trials literature, the, the longitudinal and micro longitudinal, the kind of like intensive day to day studies that are out there that are able to kind of disentangle the direction of this relationship, we tend to see that sleep problems be get pain problems more often than, than the other direction. Yeah, no, Patrick, sorry to interrupt there, but I can tell you, you know, absolute certainty that that's the case. In fact, I mean, we know part of the, the way that we make decisions and what type of interventions we're going to do for pain management is, you know, the question we ask, well, how do you sleep? And, and I think that even us as physicians, we're only trying to starting to understand that if even, but, you know, the understanding is again, it's going back to that bi-mechanical model, you're like, okay, you have this pathology, whether it's a disc herniation or a fracture somewhere, and that's why you can't get comfortable in bed because of pain, and that's why you're not sleeping. But what you're talking about, hey, it's it's the opposite. So yeah, I'm sorry to interrupt there, I just wanted to kind of. Yeah, it's good to see that there's some concordance with what, what you're seeing on a, you know, in the clinic. And yeah, so, so that has formed the basis of a lot of research that has attempted to treat sleep as a means of improving pain. And so what I can tell you about that, that work is that it's very unfinished and, and I find this kind of fascinating, right? So we can look in the experimental and the longitudinal observational literature and see this directional path that we just talked about, sleep problems leading to increases both in acute pain sensitivity and into the development of chronic pain over time. That data is really clear. So the presumption then would be, well, if we treat sleep effectively, are we, are we then going to see a downst, we would, we would assume that we would see a downstream benefit in pain. And interestingly, there have been, I don't know, seven, eight, maybe a few more clinical trials of various cognitive and behavioral approaches to treating sleep. And in particular, insomnia, in patients with comorbid chronic pain and insomnia. And these trials have have attempted to employ CBT cognitive behavioral therapy for insomnia in these samples. And they've shown almost uniformly that CBT for insomnia is very effective in treating insomnia in patients with these comorbid disorders. It is for reasons that we're still working out and I think are kind of fascinating and point to some potentially interesting mechanistic discussions. It's much less effective in solving the pain problem, right? So, so we're learning from those, those studies that even though we know that there's a strong link, the resolution of sleep related pain problems is not happening just by improving sleep. And so that's led us to really narrow in on, well, what are these kind of intermediate mechanisms that are taking place and should we be taking a kind of more complex view of the scenario? I'm focused on affective mechanisms, reward-related mechanisms. And I think if we start to, you know, darsh getting into your point earlier about precision medicine, taking more of a precision medicine approach to this sleep pain problem, we're going to, I think, start to find kind of focused and targeted therapies that can help folks with one set of constellation of symptoms that may not help another set of folks and we can tweak our interventions and tailor them for this other set of folks who have another constellation of problems because we can only presume that pain and even the sleep pain dynamic isn't happening in a vacuum, right? That there are these other kind of symptom complexes that are taking place that may be maintained if we don't focus on them as well. Yeah, I mean, that's really awesome. Patrick, do you know in terms of, you know, you said basically that the traffic is flowing a little bit heavier towards one direction and if that literature was able to tease out, you know, whether it's new incident of pain, like for instance, does it decrease the threshold for somebody to experience pain with another incident that they might experience the next day or is it more that it's increasing the intensity of a current pain condition? We've seen both. So there are, there are longitudinal epidemiological studies. I'm thinking of a couple that I believe came out of Norway over the years that have shown that insomnia symptoms at baseline predict new onset, new incidents of chronic pain down the line. And then there are studies in patients with chronic pain where we look from day to day at their sort of variation in their sleep continuity, for example, the degree to which they are achieving total sleep time consistent with their average or sort of maintaining sleep continuity throughout the night, sort of not having a whole lot of wake after sleep onset. And we can see that nightly elevations in these and things like wake after sleep onset promote increases in pain the next day and people who already have kind of chronic pain on board. And is there a difference between whether it's sleep onset in insomnia versus sleep maintenance in insomnia or is it just, is it all categorized under one? No, there are differences and those are two kind of categories, right? So you've tapped into two categories of insomnia. And I can't say that the literature is sort of resolved with respect to whether one versus the other is more important for chronic pain, for example. We've been particularly focused on sleep maintenance in insomnia and measuring kind of aspects of sleep maintenance insomnia in experimental paradigms. And so that's been a particular focus of bars, but I think the literature is probably undecided about one versus the other. Yeah, and I think it's worth mentioning though, what we know for certain is this sleep has a profound effect on performance. When it comes to the performance in sports and obviously the literature is pretty clear that when it comes to injuries, you are much more susceptible to injury looking at not only the athletic population, but even just the lay population. So I wonder if they controlled for that to see if there were any new injuries or if that kind of included that. That's a great question. I can't say the work that I'm familiar with actually doesn't get into sort of injury too much, but that's a fascinating angle. What have you seen in that regard? Well, I mean, we know that obviously hamstring injuries are extremely prevalent when it comes to just any type of field support, any type of sprint exports. And I want to say I could be misquoting here, but there was some work done from this lab out in Stanford. They're talking about how sleep impairs or the risk of hamstring injuries kind of forget how much the increase is, but it's markedly increased after just in sleep deprived individuals. And these were subjective scores, self-reported kind of what we had you had talked about the diary and stuff. I don't remember exactly how they tracked it. And obviously a lot of the work has been done in BA players because they travel from, you know, whether it's East Coast or West Coast and they're kind of getting late to the hotel and then they have a game the next day so there's sleep deprived situations. And so there's a lot being discussed in the professional realm on that regard. So yeah, I mean, it's truly fascinating stuff and we're starting to, I do love the fact that we're starting to appreciate it more and talk about it more, but I mean, there's just so much to learn and so little we know. Completely. Yeah. Yeah, I wonder what's going on in those, you know, professional sports teams. I've seen that I think many of them do have kind of sleep specialists on board now, but I would love to see kind of what the protocols are. I'm not too are they publishing that type of thing in the academic literature? I have been have you some? Yeah, I mean, some of it. I think I don't know about the professional level, but I know at the collegiate level it's being published. I think it's a little bit easier to get access to that data obviously for university athletes. I don't know too much about the professional, but I wouldn't be surprised at least in I feel like Europe is ahead of us when it comes to this type of stuff. So I wouldn't be surprised if we had some some good data on like soccer athletes. Yeah, I think maybe like a year or two with the NBA because I know that's a huge issue in the NBA now that they're really trying to track down. I think some of the stats they were saying is like NBA players might sleep at like 12 a.m. just giving jet lag and things and then wake up around five just going to work out in and they've really seen the injury rate go up because of that, especially with the amount of games that they're playing. So I want to be surprised if we start seeing that data in about a year or two. Yeah. So I also wanted to ask you Patrick about the opposite of insomnia. Is there anything that shows us that you can also have too much pain if you're sleeping too much or is it really only just kind of that insomnia state? That's a good question. And I'm less familiar with the sort of hyper-somnellance literature. I know there is one out there. It is I can say it's not the it's not a sort of primary focus of the sleep and pain literature largely. The vast majority of that work really focuses on the loss of sleep in various ways in which you can lose sleep. But you know the hyper-somnellance I think tends to focus on you know affective problems that emerge in the context of sleeping too much. And I believe there there are some data with pain but I'm not familiar enough with them to be able to to talk about it. Yeah I mean I wouldn't be surprised if there was to be honest with you. I know that I remember that again there was a paper I was looking at and I think it was a journal of in cardiology talking about how less than six hours of sleep there was significantly higher mortality associated with that. And then the same was true for sleeping more than 10 hours. And I remember you know Matthew Walker gave a great explanation for this basically talking about how individuals who spend more time in bed you know it was basically that they might be they might be fighting a disease process and in your body is he describes as the Swiss are the Swiss Swiss Army knife that you have to fight end disease essentially is to sleep. And you know in these individuals basically your body is telling you to fight this this disease process you should sleep more but unfortunately sleep failed and then they died. So it's kind of hard to tease out and I wouldn't be surprised in individuals who are spending more time in bed because they're you know in this anodonic state or because they're depressor and whatnot and and again going back to the idea of hey there's a high correlation for just your experience of pain when it comes to that type of stuff yeah but yeah I mean that's kind of what what makes this super awesome. Yeah yeah I think that that's that's certainly an interesting angle and I think the thing to tease apart and some folks may be doing that this I'm not I'm not familiar but the thing to tease apart would be to what extent is the hypersomnellance a sort of secondary aspect of an anodonic process that's going on versus a physiological kind of drive to sleep 10 or more hours that would then be related to subsequent pain I think that would be the thing to try to figure out. Yeah absolutely so how do you like when you get somebody in the lab I mean I know that you kind of actually I want to go back to about the sleep trackers that you talked about you touched on actigraphy and darshan got his whoop on I have an aura ring I'm a fan of that just because of his low profile but what are your thoughts and sleep trackers in general in terms of their accuracy and obviously we know the gold standard is you know getting into a lab and polysomnography polysomnography right just sleep trackers in general what are your thoughts? Well they're they're certainly useful they are making people much more aware of their sleep across our society than we probably were before they came about and you know I think I have a whoop too and I I have a hard time just wearing things on my wrist so like every time I've tried I tried with a Fitbit I've got about like a three month shelf life for these things and they sort of make their way off my wrist so maybe I should try the aura ring maybe maybe the finger is a little easier to deal with yeah in general I think they they are great they're great sort of everyday clinical tools and they make you know doing research a good bit easier we have sort of quote unquote research grade actigraph devices that you know are probably not all that much better than the commercial devices that you can get now so I think the commercial space is really catching up in producing pretty high quality devices I think the the thing to look out for clinically I guess as a psychologist this is where I go some folks will become so overly reliant on what their kind of sleep scores looking like day to day that they may they might infer more into individual data points than maybe would be necessary so that would be the thing I would look out for clinically for example you know some of these devices will will provide sleep staging with and they'll claim very high degrees of accuracy on their website and then it's kind of hard to figure out whether you know how truly accurate relative to for example a lab PSG these devices are actually becoming but assuming that there even there is some degree of accuracy you know you can have patients who might get really freaked out because they're noticing that their slow wave sleep is you know less on a few nights out of the week and then that might drive their behavior in a certain way and so I would kind of I would be a little bit worried about putting too much credence and individual data points but I think the ability to track I think is balanced and and and then some by the ability for folks to really get insights into their sleep habits and and things like like doesn't the whoop kind of tell you if you've had something to drink a little yeah exactly it reminds me that there's like a journal in the whoop and you can put oh I wore blue blockers or I drank some alcohol or I slept in the same bed or I had stress and then it'll even break it down to how how much earlier you know do you need to do those activities to either show a positive effect or a negative effect on your sleep yeah but I did I did have a question about that so with these sleep trackers having these journals a lot of people are resorting to you know breathwork meditation things that might show a positive benefit on their sleep is there anything so I think we know that during sleep it starts to solidify those patterns that we have during the day especially through learning and things like that so when it comes to pain is there anything that you really recommend that you know people can do to kind of decrease their pain because when they go through sleep it's going to kind of form that neural circuit to decrease their pain yeah well I think that's a good question so the first thing to try to figure out is is there a sleep problem on board and then you can you can try to approach whatever the problem is through the variety of of behavioral I would go behavioral first and then potentially cognitive if if a person is in a position to work with a cognitive behavioral therapist and we can we can I'm happy to talk about those strategies if you would like I think you know for somebody who's in pain who doesn't necessarily have sleep problems I'm not aware of any kind of particular practice sleep related practice if there's not a set of problems on board that one might engage in to try to have less pain the next day I think the the scientific literature anyway doesn't doesn't have that kind of level of granularity but you know the things that we look out for and people who do have sleep problems are one of the key areas is what we call stimulus control and and that is we we don't want to associate the bed with really anything but good sleep like if you're having sleep problems you want the bed to be like you're safe haven like when you see it it should it should sort of trigger us comforting thoughts and thoughts of about ready to crash and what happens very commonly is that people who develop insomnia and and related sleep problems will start to kind of associate the bed with tossing and turning all night and that's when we if we're working with somebody clinically will help them kind of develop a system for recognizing when they've been tossing and turning for a certain period of time and then really systematically and rigorously sort of sticking to the plan of getting out of bed and not having that period of hyper arousal be associated with the bed and if you can stick to that it it's sort of part of the constellation of techniques that typically you know resolved and it's going to get a little bit worse before it gets better but if you can get through those periods of a few nights where you're kind of like awake and staying awake on the couch and out of the bed and going through that process eventually you can kind of retrain your brain to associate your bed with with good sleep and only be in there when you're like truly ready to go to sleep now Patrick would you so I think that we can all agree I'm definitely interested in learning some of the techniques that some one might use in CBTI but obviously sleep hygiene is probably first line treatment like we would talk about you know again wind down routine making sure that the lights are all you know all you have here in our dark room it's a cool room I think those are things that people have probably heard about but what are some other CBTI strategies that that one might employ to address you know either any type of insomnia that somebody might experience yeah no you're right yeah you want to like take care of the low hanging fruit and the sleep hygiene stuff is is generally that it's important I think to distinguish sleep hygiene from CBTI right so sleep hygiene are aspects of sleep hygiene are a part of CBTI a sleep hygiene intervention alone is not a CBTI intervention and I think so you you kind of you got it right exactly the way you explained it I think a lot of providers may not appreciate that distinction and might think that sort of recommending sleep hygiene might be sufficient for somebody with an insomnia problem to start to get a hold of their sleep and generally a sleep hygiene standalone intervention is going to fail to do to achieve those goals if that's kind of all that happens it can it can work for people with generally with like subclinical issues and might might fix as I said some low hanging fruit but people with like you know severe primary insomnia that's that's not going to cut it and that's where we get into the the sort of set of techniques that are commonly involved in in CBTI and so those those will include stimulus control as I mentioned where you sort of habitually force yourself to go somewhere else other than your bed when you're not able to sleep there's also a sort of systematic process of sleep restriction that's a component of the CBTI therapy and and that's again a kind of systematic restriction of sleep and scaling back to your normal sort of gradually scaling back to your desired level of sleep when you achieve certain benchmarks of sleep efficiency and the whole point of sleep restriction is really to kind of generate that drive to sleep again you kind of present it to patients as it's going to get worse before it gets better and so patients really have to be on board with the idea that really kind of properly engaging in a in CBTI is going to you know for a week or two you know result in feeling completely unrested because you were literally restricting your sleep like multiple nights in a row but it can have profound effects and it's that's just the behavioral component that's what I find actually so fascinating about CBTI is really you know with a lot of folks just that behavioral component can can really dramatically improve improve their sleep by physiologically driving folks to the point where you know they kind of are able to reset their system and so you kind of scale back gradually until you achieve sleep efficiency benchmarks one of the key techniques is you you typically will pick a wake time that is kind of your ideal wake time one thing the folks with insomnia often do is you know they'll have a few nights of bad sleep and then they'll have a night where they're actually able to sleep and then they'll sleep through until like 10 a.m. to be able to recover that lost sleep that might feel good on that morning where you sleep until 10 a.m. but it's like completely feeding into the cycle of insomnia and so and so what what we do in CBTI is you typically will choose a wake time that's like your desired wake time and then you restrict sleep up toward that and then scale back the bedtime so if your desired wake time is 7 a.m. you might restrict sleep you know you might make it so that your sleep time on the first night is 2 a.m. and then you kind of walk it back you know 145 130 and you walk it back to what till you get to you know eventually your desired point of whether it's eight hours of sleep or seven hours of sleep whatever it might work for that individual those are the behavioral parts Patrick that sounds like I mean I find this to be fascinating because it's a pretty counterintuitive approach right if somebody has insomnia and they come to you and they're like oh well I'm not sleeping well I don't get enough sleep and you tell them okay well we're gonna cut your sleep down and they're like that doesn't make any sense I should be going a bit earlier or I shouldn't be waking up later so I imagine that's got to be a last line part of CBTI right because it sounds like a miserable experience depending on how long you do it for no it's actually like the first line yeah yeah that's that's where you go right to start in fact you know the cognitive stuff will typically come later and in some folks you might not even need to do it the cognitive work is based on the the premise that a lot of folks with insomnia have this kind of hyper arousal around bedtime so leading up to bed they'll develop a state of arousal that's greater than what they were in kind of during the day and it's kind of this approach to bed that all of a sudden starts generating arousal and that tends to be associated with ruminative thoughts anxiety related thoughts and and the cognitive component of CBTI can work with folks on kind of negotiating that that type of thought pattern in and around bedtime but but yeah I think a lot of practitioners will will go with the behavioral work first and it's it's a bit of a tough cell some some patients you know are going to tell you right off the bat that they're not into that but if you can get by in from patients it is a really a remarkable treatment because there's basically no no side effects certainly no long-term side effects and it has as good as and generally and there are certainly a few studies that suggest better efficacy than any of the pharmacotherapies that are out there to treat sleep so it is a frontline recommended treatment for that reason and it's really one of the only you know if you look across all of the other most of the other sort of complex complex disorders that have a prominent kind of behavioral component to them a CBT-like intervention is generally going to be considered like an adjunct like even with pain even though pain CBT you could argue for a lot of folks that a CBT-based intervention should be a frontline intervention but you rarely hear it talked about in pain circles in that way it's typically considered a kind of a complimentary approach or something that should be worked into a multidisciplinary approach to treating pain with CBT-I it is it is a recommended front yeah I just want to say my father actually probably had insomnia for about a year and a half now for the last two months he exactly went through everything you just said where this the psychologist was tightening his window from probably like 11 30 12 a.m. to about 5 a.m. and then slowly walking it back like he said and then the whole hyper arousal wherever he was waking up he would either do meditation breath work or get out of the room and come back in and you know a lot of it he realized was you know he was scared for his life thinking you know I can't fall see for a year now he started to realize that this was just a lot of anxiety kind of in his head building up and you know finally he's he's got back into his routine but you didn't mention ideal wake time an ideal bedtime is there a way that people can find out those those two times well you know you usually pick the wake time based on your circumstances right so if you're somebody who has an infant in the house who's waking up every morning at 5 30 in the morning you wouldn't choose you know a wake time that's at like 7 a.m. that's just not going to serve you all that well so so typically you kind of you know and similarly you know work schedules and all kinds of other things are going to dictate people's wake time so you know often that's that's kind of you got to work it around the practical realities of life and and then you know the bedtime should be that gets into maybe a more interesting discussion of like so how do you so if you if you're picking your if your wake time is more or less picked for you on most cases by the environmental circumstances that you find yourself in how do you how do you decide what your bedtime should be how do you know whether you're you're somebody who is like perfectly cool sustaining on six hours of sleep versus somebody who really needs eight hours some people that might need nine hours right and and that's that's a trickier thing to figure out particularly when you're in the throes of insomnia and and I would argue that the probably the best way to go about that is to get yourself to the point where you're able to sort of consistently achieve a continuous night of sleep night and night out and then really be tracking your sleep continuity in diaries or activity and and then be completing self-report measures during the day to get a sense of your level of sleepiness right so you want to kind of correlate how much sleep you're getting at night with how sleepy you're feeling during the day and if you're if you're somebody who's consistently getting seven hours of sleep a night and all of your buddies are operating perfectly fine with five hours of sleep and you're like why do I feel you know what why do I feel like taking a nap all day I'm getting seven hours of sleep maybe that's because you're you're somebody who really needs eight hours of sleep and you should be titrating up yeah you're talking to a bunch of residents and that's the irony of the situation Patrick so I you're talking essentially about when you're talking about timing is the the concept of chronotypes right and I think most people are familiar with you know night owls or morning larks um certainly back to the idea of when when individuals come to your lab and you're looking at you know sleeps effects on pain and you're doing these sleep deprivation studies do you allow individuals to kind of just sleep whenever they want to sleep and wake up whenever they want to wake or or because again that idea of somebody who's I just natural chronotype might be they'd like to go to bed I remember my my medical school roommate would like to go to bed at two three in the morning and then wake up like 10 whereas I was the exact opposite so how do you do that I mean how do you how do you decide which hours are going to sleep in when you're doing the sleep deprivation studies when when we're doing the sleep deprivation so that's a that's a good question um typically we uh rule people out who have kind of major circadian rhythm sleep disorders um that being said what you're describing probably isn't like a circadian rhythm disorder somebody like uh your uh your roommate could have ruled into one of our studies um and we we've got a sort of control for that in our analyses so that part of it is just kind of like a practical thing it's very difficult to uh um to perform these types experiments across people they need to be standardized and uh you know just like the the timing of everything we typically go for a standard bedtime and a standard wake time and then we'll control for uh in in our statistical analyses for variation in chronotypes we we pretty much always measure chronotype and we'll get a sense of who's a larkin who's now um but if if we could conduct the perfect experiment then we would probably shift every night depending on somebody's habitual uh sleep times and then start the experiment at that time we haven't been able to do that just because of practical reasons but that would probably be the best way to conduct it yeah so just again going back to that idea of you know sleep and pain um you mentioned some epidemiological studies and just talking about the association for individuals who already have insomnia and then their perception of pain what about maybe not necessarily healthy individuals but individuals with healthy sleep um and then you deprive them of sleep um is that where the the information about hey they're more susceptible to having new incidence pain is that where that comes from a lot of those studies really most of them yes um uh we are attempting to conduct one of the first studies right now to do sleep deprivation in patients with chronic uh low back pain as you know um but the the majority of studies are with healthy subjects and we look at experimental pain sensitivity yeah is there a specific like are you just again curtailing the the total sleep time and you kind of going for that quantity or there are certain stages of sleep that that will affect so you you can uh there are a number of ways to do these types of things are our studies um we we've typically employed a method that uh is called sleep continuity disruption um in which we uh uh essentially have eight forced awakenings over an eight hour sleep period so we we wake people up each hour at a sort of randomly determined interval and keep them awake for a portion of the hour uh and then allow them to go back to sleep and then wake them up again so it's uh it's this kind of repeated awakenings model it's a pretty um it's it's kind of like a blunt hammer to the notion of uh sleep maintenance insomnia people with actual sleep maintenance insomnia rarely have that many awakenings or force or or you know find themselves um uh disrupted that severely but uh it gives us a sense of really kind of the acute effects of something like that and there's other ways to do it too a lot of studies do total sleep deprivation where you'll see for example 36 hours of total sleep deprivation or more in some cases um you you will see sleep restriction uh where you'll just uh scale back the sleep time uh and you might allow people only a four hour sleep opportunity period but that sleep opportunity period is a continuous one and then there are other uh there are more complicated designs where you can be tracking people's sleep stage in real time and wake them up when they enter a certain sleep stage that's a really tricky type of uh study to perform but um it it has been done um and and then there are some kind of more elegant uh uh pharmaco uh uh disruption designs where uh you there there are certain uh uh pharmaceuticals i believe is it uh oh man i'm gonna i believe it's clonidine um all right i'm gonna have to pull pull this study and give it to you um there uh there are certain uh pharmaceuticals that can for example wipe out like REM sleep without disrupting total sleep time so you can achieve a full eight hours of sleep uh but not get any REM and really reliably expect that effect um with the drug on board um and that's kind of a really nice and elegant way to to just kind of wipe out one stage of sleep and and sort of mechanistically test questions that you might have yeah i i'd love to see that paper because i mean clonidine is a pretty common medication that we use for hypertension and a couple other things even for in states of pain actually um CRPS we sometimes use it for that um yeah that that would be cool it's probably not clonidine either way whatever it is that's what i'm trying to try to avoid for sure well Patrick this has been everything you've been talking about has been super fascinating especially your research just for lack of a better word awesome to me um in this field of pain and sleep mental health that we're looking at what is the direction of this field where's it going is there anything on the cost that we're looking at anything on the horizon uh yeah lots of things um so we are uh i can tell you about the studies that that were interested in um you know we're really interested in the uh effects of sleep on as i mentioned earlier these uh kind of reward related processes and and their implications for pain and one of the uh and we're interested in kind of two key areas with that one is um you know do we see that sleep problems alter uh motivation the ability to engage in naturally rewarding activities and if we can demonstrate this and we're starting to if we can repeatedly demonstrate this and bring into the context of pain self management i think that that's a uh an area that's right for uh uh building uh novel treatments um and why in that particular way you know we have these really great um uh pain self management interventions CBT for pain is intended to help give people the tools to manage their pain on a day-to-day basis um for example uh and there are you know uh various meditation practices um that can be really effective one of the key components of really all of those interventions but particularly the CBT related pain interventions requires motivation to stick to the plan right so uh when you're asking a patient to engage in um you know mild exercise on a consistent basis we've got to have the motivation to get up and do that and to overcome whatever obstacles might be in the way um and so we're really interested in seeing if uh sleep problems make it harder for people to effectively engage in those types of therapies and if we can incorporate uh uh sort of uh either interventions on the sleep side or interventions on the affect and reward side uh in the in folks who have sleep problems we're hoping to sort of break that cycle and and be able to help people more effectively engage in their own management of their pain um the other area that that uh we're excited about generally in the sleep reward and pain um spaces is in uh the context of opioids so in in patients with chronic pain who are prescribed chronic opioid therapy um and then also patients with opioid use disorder who have comorbid chronic pain and comorbid sleep disorders um uh they're uh with regard to that that group of folks uh with OUD there are very few treatments available um that uh that can help them manage that kind of constellation of symptoms while also managing the risk of relapse um and and uh and we know that pain and sleep problems uh uh will contribute to uh the likelihood of relapse in in patients with OUD so that's something that is really commonly reported by uh by patients and that we uh we see clinically and there are some research findings starting to come together looking at that so um uh we think that uh treating sleep uh in patients with OUD might be able to help them uh uh manage uh not only some of the behaviors associated with addiction but also uh might manage might help them manage pain uh and manage their emotions on a day-to-day level that uh ultimately can can result in better outcomes well Patrick um you know as uh as we approach all of our bad times we've been talking about sleep for the last like 45 minutes or so I think it's only right then out we don't miss out on any of our sleep tonight um but before we let you go how do how do people find you how can people find your work if they're interested in good good question um uh well you know I'm I'm on the Hopkins uh Department of Psychiatry website uh I've got a Twitter handle not super active on it but getting more active at p underscore five um and yeah and uh yeah we have uh uh I would say look me up on the Hopkins uh psychiatry website and you can find a link to my stuff love that and we can throw them this show note for sure oh Patrick I want to thank you so much uh for your for your time being so generous and definitely dealing with our typical difficulties here um I think this has been a great primer um and you know these complex topics of both chronic pain and sleep um I mean we know that sleep is kind of the the bedrock you know for when we're talking about the foundation of just good health and you know we've spent a lot of time talking about nutrition and exercise and just coaching in general and this is uh one of our very first discussions of sleep but I suspect they won't be our last so thank you so much for your time awesome thank you thanks for having me on all right all right well that was an awesome show with doctor Patrick find it but before we end don't forget to reach out to Larry Keller of Physician Financial Services for your disability insurance needs he's been around for a while in many physician communities helping them with the coverage they need find Larry at doctorpodcastnetwork.com for slash Larry Keller all right guys time for that quick disclaimer everything in this podcast is for educational purposes only it does not constitute the practice of medicine and we are not providing medical advice no physician patient relationship is formed and anything discussed in this podcast does not represent the views of our employers we recommend that you seek the guidance of your personal physician regarding any specific health related issues and again as always if you really enjoyed this podcast or you like the other episodes please please great review subscribe and share and spread the love until next time