Sleep medicine specialist Rochelle Zak, MD, delivers a rousing update on what’s known about sleep’s stages and physiological payoffs, followed by her guide to assessing and treating insomnia – by far the main sleep issue seen in primary care. Learn what to do with a patient’s Fitbit data; how to discuss “sleep hygiene”; how CBT for insomnia works; and uses and caveats for the range of drugs used to help patients snooze. Bonus: Tips on understanding and addressing sleep apnea.
Um, first off, I want to thank you. It was a great deal of fun making this lecture. And, um, what I did when preparing it was actually talk to my 25 year old son who has a degree in engineering physics and his friends, as well as reflect on what's the patient population from you whom I see. And so I'm sort of extrapolating. So yeah, I'll talk about sleep apnea, but not for a long time, because that's actually probably much less of What you see then um some of the other issues. And so I will talk about top sleep issues, but I do want to address apps and naps, because that's what these kids ask about. Um, whoops, OK, just when we said we did a whole trial. Yes. OK. Um, so I have no disclosures. I'm going to, at various points in time, talk about a little bit of physiology, so you know what I'm talking about non-REM and REM. And then I want to talk about the wearables, because they all come in and they want to show me their aura data and their Fitbit data, etc. um, and what are, what's helpful from it and what are the limitations. And then, I wanna start with insomnia, because that's the #1, 2, and 3 diagnosis that we end up seeing. Um, to really explain to you a lot of the behavioral treatments, what they're doing now, and there's some very nice summaries in the literature, then I, you can't do a sleep talk and not talk about sleep apnea, but that's probably not a lot of what you see. And of course, um, as Doctor Kim alluded to, I can talk about restless leg syndrome for hours. So luckily, there's a 45 minute limit on this. Talk. So we'll get to what we can get to. And if you have further questions, please ask cause I can wax eloquent forever on RLS. OK. Um, so the first thing, um, is to understand that, how we define different types of sleep. We grossly, and you probably all learn this anyway, divide, divided into non, I'm sorry, let me just go back. This is a sleep hypnogram. It is a graphical representation of sleep changes throughout the night. This would be the beginning of the night, the end of the night. These are the different sleep stages, wake, REM, and then 3 stages of non-REM sleep. So sleep is grossly divided into REM and non-REM. And within non-REM, we divide it into drowsy, light sleep, and deep sleep. And depth of sleep is defined by how hard is it for me to wake you up, how loud a bell do I need to ring, how painful a stimulus do I need to impose to get you to wake up. And you can see that non-REM and REM leapfrog throughout the night, but the other thing that's important is where they occur. So REM starts out, the first REM episode is very short, and it's your last REM episodes that's actually your longest. This person was woken up, it probably would have extended about 40 minutes to 1 hour at this point. And you see that as you leapfrog throughout the night, the amount of deep sleep goes away. And in fact, most deep sleep is during the 1st 3rd of the night. Now, why am I showing you this? Partly because I will continue to talk about non-REM and REM sleep, and partly to address the question that these kids want to know about, which is, should I nap, or what, what's advised for naps. And you will, and Whether or not you basically need the amount of sleep you need to feel refreshed, and you need it over a 24 hour period. So in a siesta culture, people are going to nap. In the American in the American culture, people tend less to nap, except now that work actually goes in. To the evening and late into the night, napping can be helpful. So if you need a daytime nap to get what you need to, to feel refreshed, we recommend that daytime naps be limited to 20 to 20 minutes is the technical. I'll often tell people 30. Now, why do we have that limit? The reason is that if you look here, when you start awake and you go through, it takes a while before you get into deep sleep. As I mentioned, deep sleep is very hard to wake people up from, and when they wake up from deep sleep, they feel as if they have never slept. And you'll, um, for, um, they always talk about the intern who's paged in the middle of the night and has no Memory of having even answered the, the, the beep, the, what's, uh, the beeper or what they said. That's because they were awakened out of deep sleep. They were groggy, and they have no memory for it. And when you wake up out of deep sleep, you actually feel worse than before you went to sleep. And that's why we say to limit it to 20 minutes with the hope that people will not enter depth deep sleep. I often say to go to 30. OK. They will always, people always ask, why do we sleep? Well, um, there are multiple reasons. We know about immunity because of the original studies from the 70s, I think it was, um, where they put rodents on a disk in the middle of a water, uh, thing of water, and the disc would start spinning, and if the rodent didn't run, he was gonna hear, it would fall into the water, and they kept running and they died of sepsis. So we know that severe sleep deprivation. affects immunity. Metabolic homeostasis, when you go to sleep at night, the temperature drops, your metabolism decreases, you know, you go from, and then you change from the sympathetic to the parasympathetic nervous system, from the fight and flight system to the rest and digest. This actually is just important to understand baseline and it actually comes up when we talk about apps. Which is that the, when you actually watch people enter sleep, you will see as they go from sympathetic to parasympathetic, that the pulse starts to slow. The blood pressure actually goes down. And so one of the problems with obstructive sleep apnea is forget even the fall in oxygen. But when you have sleep apnea, you have frequent intermittent arousals. That's how you end up, um, As ending a respiratory event, and with each of these arousals, you end up going back from parasympathetic to sympathetic, i.e. you get a burst of sympathetic activity with an acute increase in pulse and increase in blood pressure. Now, why else do we sleep? Memory consolidation. And the interesting thing about that is we, is that we have now learned that every single sleep stage is important. There isn't anyone that you can afford to, to not have. And so you Sort of divide, there are all sorts of types of memory, and I know that there's some PhDs and CITES, and they probably know this so much better than I. But just grossly, if you sort of think about procedural memory, which is how you do something, learning to play an instrument, um, memorizing physical types of behaviors, as opposed to declarative memory, which is facts, light sleep, we need for procedural memory. This was a lot of the work that Matthew Walker did when he was doing various nap studies on Cal students. Um, Deep sleep is fascinating. We had no idea deep sleep is playing a role in memory. So, as I told you, deep sleep, hard to wake people up from. It turns out you need that to have to for declarative memory. So, we learned a few things are happening in deep sleep. Um, this is, um, these are data out of Um, Italy, Tonini, I think it was who defined it. Um, pruning is the term they use. And the idea is that while you're awake, you are having experiences, and they're getting encoded in various neurologic networks while you're awake, and you don't want to run out of room. And so you have to prune back, get rid of the ones that aren't impossible to allow for storage the next. Stay. Literally, deep sleep is defragging the hard drive. And we also now know about GLMF. The brain does not have lymphatic channels, it has lymphatic channels which wash away bad things, waste products, and these tend to be more open during sleep. REM sleep, we've known for a long time that was necessary for memory, so that's much less, um, revolutionary, and you need it for both. You need it for declarative and procedural. But here's the thing, how did, one of the measures of antidepressants was how well did they suppress REM sleep. And so people can be on we know that you can suppress REM sleep to some degree and not have an effect on memory. So we know you REM for memory, um, but it, the, we don't totally understand this because we do know that with REM suppression, you can improve mood and not necessarily have an adverse effect on memory. So there you go. Um, now, I, I wanna start talking about apps and in order to understand their limitations, you have to understand what, how we have defined sleep. And what we look at in the sleep lab. So this sort of shows you what a person who's in a full polysomnogram, which we can hardly ever get paid for anymore, um, but we, we do a modified EEG and we actually do 6 to 8 channels depending how you look at it. We do frontal, central, occipital. We put eye channels here because that's how we define rapid eye movement sleep, right? Eye movements. And we also pick up EEG. Here actually, which is why I said it's between 6 and 8 channels. Then, so, and then we do chin tone because in REM sleep, the chin tone drops. We also are able to measure um respiration with bands across the chest and stomach, and measure nasal airflow that sits in the nose, pulse ox, and we actually, there are leg leads here that will monitor leg kicking. Um, and we actually, um, I'm sorry, let me just go back for a second. We also have video. I love having video. Because one of the limitations with home sleep tests is that this is back, this is side. What's this? I can see this on the video. I can see a head turn, and that can be the difference between diagnosing positional sleep apnea and not, but I'm gonna get off my soapbox now. So, this is what an epic, i.e. 30 seconds of a full polysom uh, full, full polysomnogram looks like. These are the data we look at when we do polysomnography. So here are the 60EG leads. the two eyelids, which also clearly are showing you EEG, your chin tone, your, um, uh, uh, it's your EKG, um, you know, your rhythm strip, one leg, the other leg snore channel. This is, um, airflow. It's actually, this is actually pressure. It's a pressure transducer, which is a very sensitive measure of airflow. This is actually nasal thermostat. It's actually measuring temperature, but it's another version of airflow, the thoracic movement, abdominal movement, and the pulse ox. OK. Now let's get to the apps. Now that you know what the gold standard is, you'll be able to understand where we get the limitations. How do you evaluate apps? It's a little complicated, because they have proprietary algorithms. So when people are doing studies on them, you, you know, you only have access to so much. Um, there are different outputs. So with respect to sleep, sometimes there's just a sleep score. Others are trying to show you percentages of different stages of sleep. What are they actually looking at? For the most part, they are doing it, they have an accelerometer. i.e., it's, it's tracking movement the way an old actigraph would. They tend to be triaxial, which is nice. Um, that means three different, you know, axes, your X, Y, and Z, but don't really ask me what that means. But it's basically a sensitive measure of movement. But interestingly, they now add heart rate and heart rate variability. Why do we care? We care because as I've mentioned, you transition from the sympathetic to the parasympathetic, i.e., there's an increase in parasympathetic drive during sleep, and in REM sleep, they fight with each other. The sympathetic starts to come in this and rest and pulse rate gets very regular. So this is helping these algorithms to understand whether or not, whether or not it's measuring sleep or wake and what stage. Some of them will have a pulse ox. There are, and so when I'm talking about these, you're talking about the aura ring, um, the Fitbit, um, the Apple Watch. They're mostly doing motion and cardiac activity, that the heart rate, the interbeat, um, interval. And um sometimes there's pulse ox data added in. Unfortunately, there are very few with EEG. Now, this is really interesting. Um, I don't know how how familiar you are with um the um the Bs and um the um said line, but in anesthesia now, they're using these strips to monitor frontal EEG to gauge depth of anesthesia, and I have been extremely lucky in one of my Anesthesia colleagues has asked me to actually look at the raw data for her. And it's good. You can really see brain waves, and you could score sleep. And that's what dream was doing. It actually was frontal and it had one occipital. They, um, they know, they used to market to the consumer, but they don't anymore. They can be used for research studies, but they've sort of pulled out of the consumer market, which actually is really the best, um, what if you really want to know sleep, you really need an EEG because This is what happens with these, um, fairly similar to the data from an acttograph actually. The aura and the Fitbit are very sensitive for sleep. And so that's good. They're gonna pick up sleep. They sort of overcall it, um, meaning, uh, and, well, let me just, uh, I'm sorry, that's down here. Um, but they're not as great about sleep stages. The aura, which will, which produces a beautiful little, um, hypnogram similar to what I showed you, actually overestimates REM and underestimates deep sleep. And when they, when it was actually done 1 to 1, comparing epic by epic with, and what I showed you, the type of data I showed you, there was only 50 to 65% agreement. Um, my only experience is that I did have a patient who's coming in for an in lab, and I told him, just wear your aura ring, let's see. And it actually did correlate with REM. But, um, but that's my one. Anecdote. Um, it, the, a larger study showed only 50 to 60% agreement. And one other problem is the ring has to know if you're going to sleep or not, and I don't remember how it does that. Actually, I don't know how it does that. Uh, but in some studies, if it didn't figure out that you were going to sleep, it wouldn't score it right. Now, it's a poor, it's poor for detecting wake. So it underestimates weight. So what this means, and what this means is that if somebody comes in and says, my Fitbit, my aura, my Apple Watch, It's telling me that I have a lot of wake during the night, that's probably accurate because it's gonna underestimate it. But it will, it will, uh, so if you have decreased sleep, this may be an indication of poor sleep. Um, but it's not 100% accurate. It is definitely not an accurate vis a vis sleep stages because patients get really worried. Am I getting enough deep sleep or whatever. Um, and it is somewhat surprisingly similar in the numbers tactigraphy. Um, but the real thing is people need to not focus on a number and not focus on this. You really need to focus on how you feel, how are you functioning. You need the amount of sleep you need to stay awake. Um, so that's kind of the story on these. They are, they, the, where they will probably end up being the most useful is in terms of gauging efficacy to insomnia treatment, and I'm gonna show you, um, and I'm gonna, when I discuss how people do sleep restriction, etc. there I think it can be useful. But for people who either don't have sleep complaints and are just curious, it may not be completely accurate. And it's not helpful to focus on this number. People get overly um focused on them, but it will end up, I think, being a useful aid, particularly with the insom when patients are having insomnia. Um, snoring, they're pretty good. They're kinda, um, and it's a nice clinical screen. There's something called the zoom function. I think Snore lab has it that will allow, cause remember, when they use these, they're gonna use them the entire night. They'll allow you to sort of zoom in to areas where you're snoring if you wanna play it back. Um, not totally accurate, because you don't know who's snoring. Um, one of the funniest talks I heard, and I can't remember who it was, but it was, if I'm not mistaken, an Irish sleep researcher whose, whose happiest moment was when he showed that the British bulldog was the animal model for sleep apnea. So I don't know how many of you have friends who have bulldogs or pugs, but the dogs with the smashed in faces faces, they're going to snore. So it can be a false positive if somebody else is snoring in the room. If the patient's facing away from the smartphone, it can be a false negative, but they can be a nice screen. But pretty much if somebody just complains about your snoring, that's actually good enough for me, because the reality is, um, number one, I kind of don't mind doing unnecessary sleep studies, and that I'd rather make sure we find people than not. The other is that in particular, Um, although women can snore as loudly as men, they tend not to snore as often. And so you get a, I've seen people with wicked apnea who just come in with occasional snoring, mild snoring, um, but it's unusual to have absolutely no snoring. Um, it can happen. But I don't care as much about how loud it is. I care more that they have snoring and, and that their sleep is unrefreshing. So the snoring. Maps are helpful, but again, it's not as necessary. In terms for sleep apnea, it's kind of interesting. There's a very old one. They're actually these mattress sensors. They go underneath the, the sheet. The, these have been around for a long time, used most, they used sometimes in the European studies. I don't know why they don't have much um acceptability here. Um, they actually are able to measure respiration and body movements. They're very sensitive, but they do have a 20% false positive rate, particularly for mild. They're also contactless devices, and they're trying to pick up changes in snoring essentially, and are you seeing crescendo and that kind of thing. Um, again, you can have a false positive, um, and then there's some that are pulse ox, again, microphone accelerometers, fairly sensitive and a false positive rate, although is that, you know, again, it can be a nice screen and then you can send someone in. OK, this is what we deal with all the time, right? Um, among ourselves, among our patients, and, um, so in order to understand that, you need to understand why and how we sleep. So the process of sleep we talk about, we primarily talk about process um S and C, and then there's also process A, which is Attention. So, I'm gonna start with Process C. Process C is the circadian drive for sleep. It's the biological clock. It gates when it's easy to fall asleep, and when it's hard to fall asleep. The biological clock opens twice. So, the, um, so the gate, the gate, it's gonna open right before sleep. This is when you have a, a huge drive for, um, This is the drive for sleep, so it's gonna open, and then, and then it's going to close, so you stay awake. And then it's gonna open again right around the siesta time, OK? That's Process C. Process S stands for sleep because sleep researchers aren't very creative, um, and it's the homeostatic drive for sleep. It says that the longer you're awake, the greater the rise of the, of the somnogens, which are these circulating, um, chemicals that will promote sleep. The major one is adenosine. The longer you You're awake, the more adenosine you produce, it'll make you sleepier. And caffeine is an anti-adenosine drug, that's how caffeine promotes alertness. And when you sleep, adenosine falls. I put this here because it's important to see the tumor necrosis factor, IL1, they also go rise and fall throughout the day. They tend not to be major modulators of sleep unless you're sick. And this is why you're sleepy during while you're sick, you get a lot of, a lot of TNF alpha and interleukin 1, and then finally we have process A which is for attention, which means that um all of these can be overridden if you are bored. Um, OK, the new guy is Orexin. You may have heard about this, and we'll talk about it with the with the DAs, the dual orexin receptor antagonists. Um, Orexin is the, is, um, the major, the major modulator. We, we sort of like to think of SLIT that The original description was that it's, it sleep is regulated by a flip flop switch. You'll see that all over, that either you're awake or you're asleep. They talk about a flip flop switch, and then they actually, um, uh, this, this, the, um, illustration is a teeter-totter, but fine, they mix their metaphors. Um, but erection that's coming out of the lateral hypothalamus is controlling it all. So, when a rexin starts being Reduced by the hypothalamus, it positively stimulates the areas of the brain. This is the, um, the tuber, the tuberoammillary nuclei in the hypothalamus, the dorso and these are in the brain stem to, to start putting out your wake-promoting chemicals which tend to be norepinephrine, serotonin, and actually dopamine. And then they inhibit the sleep promoting and then when they erect it stops being promoted, then you end up having the um you have the sleep, the sleep promoting areas of the brain starting to put out the more inhibitory neurotransmitters of GABA and galanin. But again, a rectum plays a role in, in supporting and maintaining wakefulness. OK, so now that you have that sort of as background, we'll start talking about insomnia. Um, they, basically, when you talk about insomnia, you talk about behavioral treatments and pharmacologic treatments, right? And I'm gonna talk a bit about both of those. Um, this is a, I was actually look, trying to find something else and I stumbled on this lovely patient summary that came out of UCSF. Um, Andrew Crystal is a psychiatrist who specializes in sleep and Most of the, not most, many of the drug, um, the drug therapy for the drug studies for insomnia will have his name on it. He's an expert on that. Liza. Ashbrook um is a neurologist who also specializes in sleep, and she's actually doing most of her work on, um, circadian rhythm disorders and Eric Crowther I'm gonna refer to him later. He is a, um, neuropsychologist who specializes in behavioral aspects of insomnia. This is just a really nice summary for patients. So I don't mean this to be self-promoting, but it's a really nice link. So when you get the slides, you can access it for patients. Um, I just thought it was really well done. Um, behavioral treatments. Don't bother to look at this, I'm, um, because it's kind of annoying actually when you know how the sausage is made. But this reference, it, um, has this. This is such a great table. Um, and so what, what we ask them to do when they did this task force is to clearly spell out each of the types of behavioral treatments. So really, this is just one of the best summaries I've ever seen. So the mainstay of treatment, the #1, 2, and 3 treatment for chronic insomnia is going to be cognitive behavioral therapy for insomnia, CBTI. It is a multi-component form of behavioral therapy that is designed to decrease anxiety about sleep. Um, align the biological clock, align the circadian homeostatic processes for sleep, which is gonna be done through stimulus control and sleep restriction. Um, to, to, um, provide relaxation techniques, which I realized I actually don't go over in this talk, but, um, I'll give you some references and also to deal with habits, i.e., sleep hygiene. Um, it was, uh, it, you know, just sort of an interesting, we're dealing a lot with nomenclature these days in medicine, right? You don't wanna say that somebody's a narcoleptic. If someone is a patient with narcolepsy, we have more patient-centered, um, language. Well, when sleep hygiene came out, and you talk about patients having inadequate sleep hygiene, literally patients would say, but I shower. And like you really have to realize, I don't even know who came up with that. I actually should find out. Not, not a great, not a great term, but um it does talk about sleep methods. And Anyway, CBTI is usually done over 6 to 8 weekly sessions by people who are trained in it. So they now talk about brief, um, BTIs, brief therapies for insomnia. You'll also see them abbreviate BBT, very similar. And then what this does is break down the individual components that actually are part of CBTI and we're really gonna talk about these in detail. Um, I actually should Um, you know what, I am gonna explain how the sausage is made for a second. We look at this. We suggest that clinicians do not use sleep hygiene as a single component therapy for the treatment of chronic insomnia. This one statement became hotly debated within the sleep community. This is where you have to really, when you look at these, you really have to read the details. Single component. What they are trying to say is that um don't just tell them not to drink coffee at night and not follow up. What they're worried about is that you'll go through sleep hygiene and never see the patient again. They are not saying that sleep hygiene doesn't work. It's very effective. It's part of CBTI. They're just saying don't just do that. Make sure you're not missing something. Make sure you follow up. So sometimes you have to be very careful and read things extremely. Carefully. So it's recommendation is against single component sleep hygiene. It doesn't mean not to do it. It means don't do just that. OK, I can now get off. I go on a lot of soapboxes, sorry about that. Um, because sleep hygiene is really, really, really, really, really, really Really important. Um, and they didn't mean, when they wrote this paper, they did not mean to say it's not. What they meant to say is there's more there. OK, so obviously, it has to be quiet. People are pretty good about that here. Exercise, people are really attuned to that. Um, they don't tend to drink as much caffeine, um, younger people, sometimes they do. Um, alcohol, what we do, do say is to avoid caffeine afternoon time to allow for two half-lives to go through. One of the things I sometimes say is people drink caffeine at 3 o'clock at night. They say they don't have any trouble falling asleep, but they end up having trouble maintaining sleep. So metabolism can vary, and sometimes it can crop up. Later, alcohol. What people don't realize is that alcohol has a soporific effect, but it has a paradoxical arousal effect when it wears off. So again, we say don't drink it near bedtime, nicotine. And the real problem is this, right? It screens, screen, screen, screens. Um, OK. So, there are probably two aspects to the problem with screens. As I mentioned, the, um, I talked about the circadian. Um, theory, the biological clock. The biological clock is, um, gates when it's easy to fall asleep and hard to fall asleep. What opens the gate? What opens the gate is the rise of melatonin. Melatonin is best to be thought of as the hormone of darkness. It rises when things get dark. It does not go up if you have light. You can suppress melatonin by light. Guess what? It's blue light specifically. So, there aren't a ton of data on, um, specifically on, um, screens and their effects on melatonin. Um, there's one article that shows that if they use screens beforehand, it shifts it a little bit later, but there are data suggesting that if you decrease the exposure to Blue light, you do improve sleep. So either putting the screen in the night mode or you'vex goggles. Let me just show you what they look like. OK. Um, a couple of hours before bedtime can improve sleep. In this study, it increased total sleep time by and sleep and improve sleep quality after a week. Um, it did, um, it decreased sleep latency, but it wasn't statistically significant. And we do know that the night mode will decrease blue light by about 93%. Here's another Um, study that restricted phone use before bedtime, um, in college students with sleep complaints, and they did much better. But it's probab light is probably not the entire story. This was actually a Frank RCT done out of out of Brigham Young, and they divided up, it's, it's large for sleep, 160. Students, you'll just laugh, but hey, we think that's large. Um, actually, the sleep apnea studies are now large. Um, but they essentially had 50 to 60 students in each group, and the three groups were no phone, phone in night mode, phone not in night mode, and they were just said, go home, you know, it was done in their dorm rooms or at home. And what was interesting was overall, they didn't see a difference, but when they looked at students who were getting at least 7 hours of sleep, Um, they saw that the no phone group did much better. And the reason they, as a, but it, the two phone conditions didn't differ. And the, so when you are on your phone, are you passive or are you active? Usually, people are on their, they're on Facebook, well, I guess they're not, they're no longer on Facebook, they're on Instagram. Um, and they're, or they're on websites, and basically going back and forth is increasing adrenaline. It's adrenaline. It's increasing. dopamine. It's increasing the hormones of alertness. So just going back and forth, even forgetting any type of melatonin suppression, is going to have a deleterious effect on sleep. They think that they didn't, and so that's what they were sort of proposing in this study was that it wasn't a function of light. It was a function of using an interactive screen. They think they did not see a difference in those who got less than 87 hours of sleep, because everybody was relatively sleep deprived, and thus everything um went out in the wash. So, it's just when I counsel people about using their screens, I say, look, yes, I know using in the night mode, that's great, but there is also a role of, of being interactive, that's actually stimulating to wakefulness. Can you just go on the Kind just get a Kindle, you know, use a Kindle or something and Read or try to do something that is passive, not active. OK. One of the main, so that's the sleep hygiene. One of the main stands of CBTI is also stimulus control. This is to align the biological clock as well as to increase the homeostatic drive for sleep. And probably the number 12, and 3 recommendation is a consistent wake time. So you're getting light exposure. When the biological clock, melatonin secreted, you open it, you see light. The gate closes and the biological clock is 24 hours and 15 minutes in periodicity and we pull it back every time we see morning light. Consistent wake time 7 days a week. Avoid naps. Avoiding naps. is so that you don't have a fall on adenosine, and you have a good adenosine whenever you sleep, the adenosine levels fall, you have a good level of adenosine when you go to sleep at night. It's also to break the subconscious association of the bed with wakefulness, and we tell people don't lie awake in bed for long periods of time. Use the bed only for sleep and sex, and it involves sleep restriction, where you actually sometimes will try to restrict their time in bed to, um, to their, to sleep deprive them a bit to build build up the sleep pressure. The other thing that happens is if people start to have trouble sleeping, they think, oh, if I spend more time in bed, I'll get more sleep. That's not what happens. What happens is you end up getting more awake. So you'll end up in, they think, oh, I'm only getting 6 hours, I better spend 8 hours in bed. And what they do is they get 2 hours of sleep, 2 hours of wakefulness, then another 4 hours. And having that wakeful, that sustained wakeful period and ends up in the morning feeling as if you have less refreshing sleep than if you had 6 straight hours of identical um EEG confirmed sleep. So really, how you feel in the morning is a combination not only of how you slept at night, but also of your experience of your awake during the night. And then they also will go over relaxation techniques. So my approach to insomnia is identify problems with sleep habits, substances, irregular sleep and wake time, personal screen use, absence of wind-down period. And then I do a lot of referral to CBTI. Um, I'm not officially trained in it. I know a lot about it. Um, I do aspects of it. But it's really best when it's done by somebody who can see the patient every single week and make incremental changes. These are just some good references cause sometimes people like Mind Over Mood, um, or Goodnight Mind, sometimes just reading that and people get enough help to deal with the, with the active mind, um, which is so, so common and particularly in this group of people. Medications. Um, there was a clinical practice guideline for medications for insomnia that was published actually um long before the CBTI. This is a much older publication. Um, they basically make their recommendations for difficulty initiating sleep, maintaining sleep, or both. Um, and so I just wanna Kind of review for you a little bit about the pharmacology of these types of medications. Um, the benzoreceptor agonists, these are the Z drugs, um, zolpidem, eszopiclone, Zaloplon. They are not gaba agonists. They actually enhance the effect of existing GABA. Now, because they are not full GABA agonists, they actually do not have an anxiolytic effect. And so I remember my, when zolpidem first came out, and I was a fellow, and I was so smart, I had this patient who was on, oh, I can't even remember what benzo was at the time. I'm going to switch her over to zolpidem. This is a great drug, and I unmasked underlying anxiety disorder. So, they are not full GABA agonists, they're actually Not gaba agonists at all, but, um, they only have a hypnotic effect. Um, one of the, they're intended for short-term use, and this is the problem is people start using them and then they don't want to go off them. They can be very helpful for things such as grief, um, you know, loss of a job, acute, acute, um, aspects of insomnia that are that, uh, um, acute insomnia. Um, one of the side effects of them is this complex sleep behavior. You'll see it described as sleepwalking. It's not sleepwalking. Um, people are, they're just, they're partly sedated. They're not sedated enough that they're staying in bed, but they're too sedated to know what they're doing. It is dose-related. It occurs 30 minutes after taking the med, and it can occur in people who've never had it years into therapy, and it's more common at higher doses, etc. Um, and And, and so those are, and they, it's not clear if they are associated with dementia or not. Um, the data sort of can, um, various experts disagree on this. Um, sorry about that, I, about the doorbell. The new guy on the block are the Doras, the dual orexin receptor antagonists. Um, these are, these are aimed at At turning the switch off, OK? They inhibit erection. So, And there are two Orexin um receptors. The, um, I didn't even put pseudorexin up here. That was the first one, Belsomra. Um, it turns out the dose at which it was recommended isn't that effective, um, which is why it's been replaced by Lemborexin Dayvigo. Um, the, and it's not that Belsomra isn't that effective. It actually just got put out at too low a dose. Um, the new one coming out is Reorexxin, I can't remember what it's name's gonna be. They tend to be pretty well tolerated. There are studies of these actually in the um in an older age group. Um, they're liver metabolized. They do not cause respiratory suppression. Um, and in theory, the, um, so it is the absence of rein that is the underlying pathophysiology of narcolepsy. So in In theory, these could induce narcoleptic type symptoms. They tend not to in most cases, but there are reports of cataplexy in patients who have been taking them, but it tends, it's pretty rare. Um, the, the other new guy on the block are the antihist, the quote, antihistamines. Let me explain what I mean by that. These are older drugs that when given at a very low dose, are just specifically an Antihistamine. One of the knocks against Benadryl is that, yes, it's an antihistamine, but it also has other side effects. Uh, uh, um, it's not, it, it's a dirty drug. When you take doxepin, which some of you may be too young to remember, was originally marketed as an anti, it is, it's an antidepressant. If you use it at very low doses, it is a pure antihistamine. And that's its only side effect. They do say to watch for anticholinergic side effects, but it's basically unheard of at this extremely low dose. Silenor is the brand name. It is outrageously expensive. So when we try to give it, we actually, there's actually um a doxepin, um, A liquid doxepin. And so we will do that and say get a dropper and you do 3 to 6 mg. What it does is it actually, it's recommended for difficulty maintaining sleep and people will actually wake up during the night, but they just roll over and go back to sleep, so they feel a whole lot better because Again, the experience of your sleep is a combination of how much sleep and wake you had during the night. Um, the other sort of newer, newer type of drug are the melatonin receptor agonists, not Remelon. It, um, there are two melatonin receptors, um, M1 receptors actually block a rexin release and can promote sleepiness. Um, and the M2 are what are used for biological clock shifting, which is primarily what I tend to use melatonin for. Um, these will improve sleep latency a bit, less, less effective on wake after sleep onset, um, and they also are metabolized, um, in the liver. Um, trazodone. Trazodone is a very old drug. Guess how good the, the studies are that tell you whether or not it works. They're pretty awful studies. And so the, the clinical practice guideline did not endorse the use of trazodone. In fact, they endorsed, they recommended against it. Yeah, the data are lousy, the data are lousy studies, it's old stuff. Um, but there's a lot of clinical experience with With it, um, it works for the serotonergic and alpha, um, and neuronergic systems. Mirtazapine, again, um, this also at very low doses is when it, um, 2 to 4 mg has a pure antihistamine effect. Um, although some people do gain weight and then of course, um, like quetiapine can be used, particularly when there's a comorbid psychiatric disorder. So the real question, so what we tend to do is I tend to go behavioral. Um, sleep is not in the pill. There are instances where patients don't do well with behavioral and they do need some limited pharmacologic. And the question is, what about the two together? And the reality is, it's probably very effective. Um, and so there are, they, um, they are working on actually developing recommendations for this. Um, it is likely very effective to give both a Med and CBTI and then as the patient goes through CBTI tapering off the med, um, the only downside with it is patients may not realize how effective the CBTI is being, um, and I, um, but it can't, but together, you can actually taper more effectively. The other thing to know is that when you are doing a taper, to warn patients that they may have a poor night's sleep for a couple of nights at the, at the inflection point when they decrease and in fact, um, Actually, Doctor Mason will actually suggest to people that they buy um these um medication scales and use a razor and slowly just keep decreasing the amount. Um, I forgot to put in a slide and mention there are, there are good data that show that in the long run, people do better with CBTI long term in terms of maintaining good sleep than if they are put on a medication. Um, and then, of course, there are the M's. Um, marijuana, the data we have, uh, so it's hard to study marijuana. Um, prior to legalization, you have to get it was very difficult. There aren't, there aren't a lot of data, but from Colorado, there was a study looking at CBD, and remember you have THC, CBD, CBN, you have vaping, you have edibles, you got a whole bunch out there. And CBD tends to have more of an anxiolytic effect, um, and this case series noted that 66% improved their sleep and 25% worsen their sleep. Um, usually people have tried it on their own, and either it helped them or it didn't. Either they had side effects or they didn't. Um, Melatonin, as I mentioned, there are two receptors, one that modulates the biological clock and one that induces sleep. The take-home point is that melatonin is a very short half-life. And that's again why Rmion is better for um melatonin receptor agonists because it's better for sleep onset rather than sleep maintenance. Um, so it'll decrease, the melatonin will decrease sleep latency, but less of an effect on total sleep time and sleep maintenance. Typical doses are 1 to 5 mg, but really physiologically, 0.1 mg is physiologic. Um, so I often will tell people try just a 0.5 mg a couple of hours before bedtime so you get this nice um secretion. There are now, there are now the um the extended release formulations. So those actually may be better for maintaining sleep, but what's important is you need to make, because it's not regulated by the FDA you don't know what you're getting. So make sure people are gonna try melatonin, that they There's one that says it's USB verified and some good ones are Naron and Sundown. OK. Now let's talk about sleep apnea. Um, you'll often see if you refer to a sleep specialist, they'll say, oh, the patient had a mala potty 4. This is what we're looking at. What we are looking at is when the patient opens their mouth, can I see to the back, OK? It's a gross approximation. This was really designed for the ear, nose, and throat docs for intubation, and we kind of took it over. Um, but melon potty form means you're gonna have a big tongue or a very low-hanging soft palate. Why do we care? All right, this is now, walk like this. So here, this is, it's a sagittal section this way. This is the soft palate and uvulae. Here's the tongue. The, the air goes in through the nose or in through the mouth, to get down to the trachea here. Here you can have airflow. Here you can't. OK? Now, we tend to associate it with obesity, but it's not all about obesity. So here's, this is a coro this is um A um uh um uh not sagittal, axial. This is an axial section, uh, an axial MRI. So here's your tongue, here's your spinal cord. This is the airway. This is somebody who's obese but does not have sleep apnea. This person is obese and does. It's the size of the airway, and a lot of that is modulated through the tongue. OK. OK. That's very important because not everybody who has sleep apnea is obese. This is actually a before and after photo of the same person before before um the mandibular advancement um and reconstruction and after. This person's gonna have sleep apnea. Because if, um, let me just go back, notice the tongue is attached to the lower jaw. What happens if you're retrognathic? Where's gonna be your base of your tongue? Back here. So you'll see it in obese and you'll see people who have either small jaws, which is gonna push the tongue back or frank retrognathia, OK? Um, so what hap, why is it sleep apnea, not wake apnea? If you think of the back of the throat as being made out of balloon-like material, it has to be actively kept open. You enter sleep, the muscles relax, it's gonna get smaller. And, um, it doesn't matter if the obstruction is complete, which is an apnea or partial, which is a hypopnea. Your body is designed to breathe, and your lungs literally are going to wake you up to, to breathe. They'll have increased respiratory effort, and there's a feedback loop from the pulmonary stretch receptors to the brain that will Literally wake patients up to breathe. They're awake for just a few seconds, too short to form a memory, but long enough to get awake muscle tone, the back of the throat opens up, you get one breath in, and immediately return to sleep. So they end up breathing at the expense of sleep continuity. So, What do I, what do we look for in the history? Obviously, um, snoring. Snoring is just vibration of the soft palate and uvula for tubular airflow. Most people who have sleep apnea will snore, but not everybody who snores has sleep apnea. So if it's loud, heard through the door, if it's been going on, how long has the bed partner been in another room. We don't see this as often because people come in sooner. Um, however, even mild snoring at times, because how disturbing snoring is, is relative. There There are now snore, as, as I said, there are snore apps that can actually look at decibels. Usually loud snoring is around 50 decibels. Um, has the, has anyone noticed apneas, gaspy or choking in sleep, unrefreshing sleep, um, night sweats generally seen with more significant sleep apnea, daytime sleepiness. We usually are seeing patients more with unrefreshing sleep rather than frank daytime sleepiness. Sleep apnea is getting diagnosed so much earlier now. We still sometimes see daytime sleepiness. It's less common. and then nocturia. And what's interesting is that the reason patients have nocturia, um, is that, as I mentioned, with each of the intermittent, um, arousals, you go from asleep to an awake state. You go from parasympathetic to sympathetic nervous system, and literally, the body starts to produce atrial natriuretic factor, literally producing, um, nature's own diuretics. So the nocturia is not simply a function of sleep fragmentation. It is also a function Of the production of natural na na na atrial natriuretic factor, forget it. Um, OK, so. Um, however, people can snore and have insufficient sleep. Not everything is sleep apnea. The differential includes sleep will be more refreshing. If it, if patients with sleep apnea, it's never refreshing because the sleep is too fragmented. I shouldn't say never. Some patients do, but generally, unrefreshing sleep. If patients snore and they always wake up and they feel fine and they're alert, that is often the story of snoring an insufficient quantity of sleep, and these patients are likely to be alert in the morning, get sleepy. During the day and often feel fine on the weekend when they get their catch-up sleep, but also it could be snoring and inadequate sleep hygiene, irregular sleep and wake schedule, and all this other stuff. Um, some people like to use the stop bang score. Again, this was developed by ENTs. It sort of gives you a like what's the likelihood it higher likelihood of having sleep apnea, high likelihood if you score 5 out of 8, and you get 1 point for each of loud snoring, tired. You can read these observed apneas. P is pressure, i.e. hypertension. Um, elevated, a high BMI, age greater than 50, neck size, it's a, this sort of is a correlate for, um, for obesity where it's depositing it here, um, and gender, it being more, it being almost twice as prevalent in men as in women, it's a 15 to 30% prevalence in men, 10 to 15% prevalence in women. Now, I am um showing you the definition of respiratory events, not because you really need to know this, but I want you to understand why the home sleep tests are not as good as the in labs, what the limitations are. Um, they're fine for most patients, but there are limitations, and the only way you can understand that is you need to understand our respiratory, how we, how we score and how we score also, by the way, we're not even sure if we're doing the right thing. First off, respiratory events last 1010 seconds, don't worry about that. Apnea. Apnea, absent breath, no airflow. Hypopnea, hypopnia, decreased airflow. Decreased airflow with something, either an arousal or a specified oxygen fall, depending on whether you're using American Academy of Sleep Medicine criteria or Medicare criteria, fine. Then you get into this part, respiratory effort-related arousals, and this is where we have issues with the home sleep test depending on the technology. This is, there is no decrease in airflow, OK? None. There's just an increase in resistance and that can be enough to trigger an arousal. You may have heard of upper airway resistance syndrome, that's based on more rarer than apneas and hypopneas, and these patients can present with unrefreshing sleep but without daytime sleepiness usually, although they can, um, but we, and this is what we see in the younger population. You, you've fallen into here. At with age. So, OSA cardiovascular issues, primarily hypertension. When you treat it, hypertension gets better. Treatment for the others, not as clear. Um, these are the home sleep tests. Uh, this measures respiratory flow. It can underestimate OSA. This is the Watpat. It's actually measuring, um, vascular tone and pulse, also oxygen, and it can conflate the leg movements that we. With RLS with, um, with respiratory events. Um, maybe I should, this is what the, this is what, this is a type 3, these are the output. Um, and treatment, CPAP, I love doing positional aids, oral appliance. Let me briefly explain bongo. This is a nasal partial nasal expiratory valve. It sits in the nose, it looks like bongo drums. There are holes with flaps on top. When you breathe in, you get full inhalation. When you exhale, the flaps go down, partially blocking airflow. That means more air goes and then goes out. It's a modified form of pap, but it's pap with expiration. We tell people breathe in and out of your mouth for comfort. Bypassing it, your mouth will close. Self-pay only, $200 for a starter kit 100. Do every few months for replacements. And again, my apologies, I really did go through this. I guess I was just talking so much more quickly when I did it at home. So tell me some questions. Let me ask that. And then I have a ton of slides on RLS and anybody who wants to talk about it, I love talking about RLS.
