The American Osteopathic Academy of Addiction Medicine is pleased to present Sleep Problems Complicated by Substance Use Disorders as a module in the online course, The Essentials of Addiction Medicine. My name is Dr. Gregory Landy and I will be your narrator for this entire presentation. This presentation begins with the review of the normal sleep cycle. While this will mostly be a refresher, it is important to have a basic understanding of the sleep cycle, if for no other reason than to educate your patients about what a normal night's sleep should look like. After reviewing the normal sleep cycle, the discussion will then turn towards explaining how alcohol affects sleep, and it does so in a profound way. Please keep in mind that I am using alcohol as the prototypical example of how other sedative drugs affect sleep, such as the opioids, benzodiazepines, and marijuana. While there are individual variations among these groups, the general principles of how alcohol affects sleep will certainly be applicable to these groups. Specific differences between these groups, such as between an individual benzodiazepine and another, exceed the scope of this particular introductory lecture, but there is information available that could help you review these particular issues also. This discussion will also spend considerable time discussing obstructive sleep apnea. Obstructive sleep apnea is often underdiagnosed, which can lead to suboptimum treatment outcomes. As with the discussion on the normal sleep cycle, we will review some general criteria for obstructive sleep apnea to heighten your diagnostic awareness of this disorder. After which, a detailed discussion of the relationship between obstructive sleep apnea, alcohol use, again as a prototype for other sedatives, and the relationship between obstructive sleep apnea and tobacco use will follow that general discussion. Finally, of course, no discussion of sleep problems would be complete without some suggestions for managing the sleep problems we've just identified. So at this point, you may be asking yourself, why is a lecture on sleep problems considered an essential topic in an addiction medicine course? Well, the answer to that question has at least three parts. Perhaps first and foremost is that among the many factors complicating substance use treatment is the unshakable persistence of insomnia. It is, after all, one of the most common complaints that all patients voice. The second answer involves issues of risk management. Relapse rates among individuals with an alcohol use disorder are at least twice that of individuals without sleep problems. Insomnia also is an independent variable associated with increased suicidal ideation. And of course, a good night's sleep is an important and, in fact, I would dare say an essential ingredient in a person's general health and emotional well-being. Take a moment and study the diagram. Here we have depicted the normal flow of a night's sleep. Sleep architecture is broadly grouped into REM sleep, or rapid eye movement, and non-rapid eye movement sleep. Non-REM sleep unfolds through three stages, one, two, and three. Which successively move from light to deep sleep. Stage three is the deepest level of sleep, the point at which, of course, it's hardest to arouse the sleeper. Another term for deep sleep is slow wave sleep. That term will become a little bit more familiar as we progress through this discussion. Again, refer back to the diagram. It's clear that deep sleep predominates in the first half of an individual's sleep cycle, with each REM episode increasing as the night's sleep continues. The cycle of REM and non-REM sleep occurs three to five times a night with each successive cycle a bit longer, initially 90 minutes or so, and then increasing to 120 minutes towards the end of the night. Another way to understand the sleep-wake cycle is to look at brainwave activity. This diagram shows the five generally accepted ranges of electrical activity. Starting at the top of the diagram is gamma wave activity, which is the fastest frequency. It occurs in the range of 30 to 100 hertz. Functionally, this is the least well-understood brainwave segment. Research suggests it may represent brain synchronicity, peak performance, or simply an artifact of non-filtered facial motor activity. Beta wave activity occurs between 12 to 30 hertz, and this range is associated functionally with wakefulness, attention, and focus. This range is often divided into three segments, low, mid, and high beta. With high beta activity functionally correlating with a decrease in concentration. Alpha wave activity occurs between 8 to 12 hertz and functionally is represented by a calm, reflective brain state, and it is a precursor to light sleep. Interestingly, simply closing your eyes will increase alpha wave activity, which of course occurs just before we go to sleep. Non-REM sleep begins with a decay of alpha wave activity. That is N1. N2 occurs with theta wave activity, which is electrical activity in the 4 to 7 hertz range. This is a period of deep relaxation. N2 is also associated with bursts of brainwave activity in the form of sleep spindles and K complexes. And finally, the deepest layer of sleep, the N3 level in non-REM sleep, is associated with delta wave activity that occurs from 1 to 4 hertz. It's also referred to as slow wave sleep. It is deep, dreamless sleep. The neurophysiology of the sleep cycle is immensely complicated and involves the interaction of numerous neurotransmitters. In the broadest sense, the sleep cycle is regulated by the circadian rhythm, which in turn is controlled by the suprachiasmatic nucleus located in the hypothalamus. The suprachiasmatic nucleus receives input from nerve cells in the retina that detect light and help regulate the circadian rhythm and regulate sleep cycle through multiple pathways that involve the release of neurotransmitters such as melatonin and norepinephrine, among many others. One of the better understood pathways by which this occurs is when norepinephrine is stimulated and released by the suprachiasmatic nucleus, which in turn stimulates the pineal gland to release melatonin. The alternating states of wakefulness and sleep are maintained through a number of neurotransmitters including norepinephrine, serotonin, histamine, dopamine, acetylcholine, and orexin. Good night's sleep is associated with certain specific physiologic changes that occur during non-REM and REM sleep. During non-REM sleep, there is a decrease in brain activity. The rate of breathing decreases as the individual descends into slower wave deep sleep. Their muscle tone decreases as they increasingly are relaxed. The blood pressure decreases. The heart rate decreases. And the body temperature also decreases during non-REM sleep. In many aspects, REM sleep is the opposite of this. There is an increase in brain activity, particularly in certain regions of the brain. The respiratory rate increases. There is no muscle tone. The individual's skeletal muscles, of course, are paralyzed. Blood pressure increases. The heart rate increases. And body temperature increases during REM sleep. But an interesting fact associated with REM sleep is that there is no sweating or shivering during this phase of the sleep cycle. The rate of alcohol metabolism is an important factor affecting its influence on the sleep cycle. The rate of metabolism is dependent on a number of factors, including the amount of metabolizing enzymes in the liver, which may be genetically influenced, the rate of alcohol absorption, which can vary depending on the presence and type of food, and other factors such as gender and body weight. In general terms, though, blood alcohol concentration peaks about 30 to 45 minutes after one standard drink. This slide shows the steady rate of elimination in hours based on an individual's blood alcohol concentration. As you can see, it's a relatively smooth decay that occurs over time. And this becomes an important factor in understanding how alcohol affects an individual's sleep cycle. Alcohol is a seductive soporific. As a sedative, it may decrease the time to sleep onset, at least initially. But tolerance to this sedative effect quickly develops. This leads to an increasing alcohol use by some individuals as they attempt to restore that sedative effect. But that launches a vicious cycle of increasing alcohol use as the sedative effect deteriorates. Now, while the person may initially get to sleep a bit quicker, the rest is often unsatisfactory. A number of factors work together to produce that result. In the previous slide, we reviewed alcohol metabolism. Now, imagine a person goes to sleep with a high blood alcohol concentration. As the night progresses, the blood alcohol concentration is steadily decreasing. In the early part of the night, the higher levels of alcohol suppress REM sleep. But as the alcohol level declines through the night, a potent and disturbing REM rebound occurs. The individual often described this as having very vivid dreams, which they find most uncomfortable. The decreasing blood alcohol concentration also results in fragmented sleep. Again, as the sedative effect is wearing off in the latter half of the night, there are periodic awakenings. Alcohol is also a diuretic, and that causes the sleeper to use the bathroom more, which of course, again, disturbs their sleep. And alcohol also interferes with the body's thermoregulation. Alcohol initially lowers the body temperature, but as the blood alcohol concentration is decreasing, the core body temperature increases, disturbing sleep. And this may also account for some individuals' complaints of night sweats. Now, let's take what we've learned so far and apply it to what is a fairly common patient vignette. So you have a patient that comes into your office and complains about their memory and their attention span. Their focus is down. They just can't concentrate like they used to. They've also been told that they are irritable. They've noticed that their mood is down. And they have mood swings or personality changes. They've also noticed that they wake up frequently to go to the bathroom. And another thing that they've noticed is that they have a dry mouth or a sore throat when they wake up in the morning. So you take all these complaints and you think about it a moment. And you have some preliminary ideas about what may be going on here. Your initial thoughts on the patient's presentation lead you to ask some additional questions. And from the remainder of the interview, you learn that the individual has daytime fatigue, which has been affecting their ability to be at work on time. They've often noticed that they nap off during the latter part of the afternoon. Really, really uncomfortable is that they've noticed that when they wake up in the morning, they have a really severe headache. After a few hours, that headache tends to pass away. But it's really quite incapacitating. And finally, their bed partner has noticed an increase in what was previously some light snoring. It's now much more pronounced and is disturbing their sleep. You now understand that your patient most likely has sleep apnea. The clues that you considered in arriving at this diagnosis included the individual's snoring, the morning headaches, the dry mouth or sore throat, the daytime sleepiness and fatigue, problems with their attention and fluctuating mood, and the presence of nighttime sweats. Sleep apnea is often undiagnosed, continuing as a significant problem for the individual. It begins, in many cases, in a mild way. And even though it interferes with the individual's sleep and causes substantial impairments in their life, it usually is adapted to, at least in the early stages. As such, it becomes a chronic condition. It definitely interrupts the sleep cycle, as we've discussed previously. And as a consequence of all this, the patient may not know that they have sleep apnea, only that they do not get a good night's sleep. There are different types of sleep apnea. The most common is obstructive sleep apnea. And we will focus our attention on this. One important thing to keep in mind is that one of the critical clues of sleep apnea is the choking or the cessation of breathing or the altered breathing that a bed partner may notice and bring to the sleeper's attention. But lacking that vital piece of information, again, the diagnosis of obstructive sleep apnea may not be considered. A conclusive diagnosis of obstructive sleep apnea relies on the measurement of certain specific physiologic parameters, such as airflow, blood oxygenation, breathing patterns, heart rate, and the individual's brain and muscle activity during their night's sleep. Polysomnography, of course, is the gold standard for determining the diagnosis of obstructive sleep apnea. But sensitive, commercially available home sleep study equipment is also used and can provide much of the same information. There are different ways to assess the severity of obstructive sleep apnea. But one of the common measures is referred to as the apnea hypopnea index. So we need a couple of definitions first. Apnea is a total cessation of airflow for 10 seconds. A hypopnic episode is also 10 seconds. But it is a restricted airflow that is accompanied by a 4% desaturation in the blood oxygen level from the baseline measurement. Those two together produce the apnea hypopnea index, which is the number of apneic episodes, the number of hypopneas, divided by the number of hours the individual is asleep. In terms of grading the severity of the obstructive sleep apnea, an AHI of less than 5 is considered normal. A number between 5 and 14 is mild obstructive sleep apnea. 15 to 29 is moderate. And an apnea hypopnea index score greater than 30 is considered severe obstructive sleep apnea. There are certain risk factors that increase the probability that an individual will develop obstructive sleep apnea. As shown on the slide, these risk factors include male, being between the ages of 40 and 70, being overweight, and having a large neck size. And definitely for the purposes of this discussion, and what we'll be focusing on, is the role of substance use, particularly alcohol. But we're using alcohol, as previously mentioned, as an example of what other sedatives can also do in terms of increasing the risk of sleep apnea. That includes the benzodiazepines, marijuana, and the opioids. We'll have a separate discussion about tobacco. It has some interesting relationships with sleep apnea that make it a special case. So as we're discovering, the use of sedatives such as alcohol, and by extension the opioids, benzodiazepines, and marijuana, increase the risk of breathing problems while an individual is asleep. So how does that work? What is happening? The consumption of alcohol in an individual that perhaps is predisposed to developing sleep apnea functions by relaxing the upper airway muscles even more so. This causes the airway to become more constricted. The snoring increases as a consequence, and the individual finds it increasingly difficult to breathe. Alcohol also has another relationship with the sleep apnea. It impairs the normal arousal response that accompanies anti-restrictive airway obstruction. This increases what is in turn referred to as respiratory effort-related arousals. So that in this situation where an individual would normally be awakened by the increased airway resistance, they do not awaken. That response is impaired, and this increases the probability that the individual will have an apneic episode. It's also interesting to note that sleep apnea accompanies other psychiatric disorders. Let's turn our attention now to the sleep problems among tobacco users. As I think everyone is familiar with, motivating individuals to stop using tobacco can be an uphill struggle. Most individuals that have a tobacco use disorder are more than familiar with the major physical problems associated with smoking, and they've made a decision to continue their habit in spite of that. I think many of us have also heard among individuals that are using other substances, particularly alcohol, that while they may be responsive to quitting alcohol, they're not as receptive to stopping tobacco, and they'll sometimes respond by saying, one problem at a time, doctor, one problem at a time. Now, what that can mean is that they're going to hold on to their tobacco use despite any subsequent treatment intervention. Now, clinicians have a choice at this point. They can, of course, side with the individual and focus their treatment intervention solely on what appears to be the primary substance use disorder, alcohol, for instance, and perhaps the future date circling back around and readdressing the issue of quitting tobacco. On the other hand, continuing to use tobacco while treatment is ongoing for an alcohol use disorder actually is problematic in the sense that the tobacco remains as a behavioral reinforcer of alcohol use. So in an ideal world, treatment would tackle both problems at the same time with the patient's full energies devoted to that. So here we have an opportunity to talk with the patient about the relationship between tobacco and sleep. I think it's fair to say that most everybody wants a good night's sleep and is frustrated when they lack it. Individuals that use tobacco will not have a good night's sleep, but they may not understand the relationship between their tobacco use disorder and their sleep problems. So this can be used clinically to help educate the patient and perhaps motivate them to reconsider quitting tobacco by focusing on what is a very common complaint among the general population and particularly among individuals that use tobacco. Now, it's interesting that of the mountains of research that have been done into the effects of tobacco, there is not a huge amount of evidence looking at the relationship between tobacco and sleep. But what we do know certainly supports the contention that tobacco use has a pernicious effect on the sleep architecture. As it would seem obvious, tobacco and its ingredient of nicotine, being a stimulant, would surely interfere with the individual's ability to initiate sleep, and it does indeed do that. The stimulating effects of nicotine also increase the number of arousals or awakenings, making it very difficult for the individual to have a cohesive night's sleep. Now, obviously, the result of a failure to initiate sleep in a timely fashion, usually within 15 to 20 minutes, and staying asleep is going to lead to daytime sleepiness and fatigue. And the net result is, of course, a decrease in the total time asleep. The relationship between tobacco use disorder and obstructive sleep apnea is even less conclusive based on the evidence. But what does seem clear is that smoking increases upper airway inflammation, which in turn narrows the airways, leading to increased resistance to airflow. Now, there's a very interesting untested hypothesis which may go towards explaining individuals' reluctance to stop using tobacco. So let's imagine for a moment an individual has an undiagnosed obstructive sleep apnea, which, of course, is causing them great difficulty in their life. And they somewhat intuitively discover that if they self medicate with tobacco, meaning the nicotine in the tobacco, that their obstructive sleep apnea is moderated. So how would that work? So nicotine, being a stimulant, raises the respiratory threshold, as a result of which it produces less sleep interruptions. And also, when you think about it, it does make sense that the nicotine that the individual is consuming throughout the day also would alleviate their daytime drowsiness. So taken together, there may be individuals that find it very difficult to give up tobacco who may be self medicating their obstructive sleep apnea. All this goes to suggest that individuals that smoke should be considered to have breathing problems until proven otherwise. Now that we have a basic understanding of how sleep problems can be complicated by a substance use disorder, we're going to turn our attention to a broad overview of how we can manage these sleep problems. Perhaps first and foremost involves managing the patient's expectations. In many cases, these problems have become chronic and will defy any quick fix. So it's important to keep that in mind and discuss it with the patient. We're also going to talk a bit about screening and assessment, bringing some evidence-based tools to our clinical understanding of the patient's sleep problems. We're going to touch on medications a bit, but the predominance of this discussion is going to be focused on non-pharmacologic evidence-based interventions that can be used with individuals that have a substance use disorder. Managing expectations means taking into account the difficulty in making the diagnosis, understanding the relationship between the effects of drug and alcohol, the sleep cycle, since these can vary during periods when the individual is acutely using them or the effects on the sleep cycle from chronic use. Effects on the sleep cycle will vary during periods of withdrawal, and even when the individual is abstinent, sleep problems can continue for an indefinite period of time. The same applies to diagnosing obstructive sleep apnea. Obviously, it would be best to make that diagnosis free of any substance use disorder that may be complicating the airway breathing problems. But, of course, this is difficult since in a number of cases, clinicians will not know if the individual is using one of these substances. So with the caveats in mind that we just discussed, let's take some time to discuss screening and assessment of sleep problems. We're going to begin that by suggesting an efficient clinical interview that will help guide your further inquiry into an individual's sleep problems. We're going to add several evidence-based screening instruments to our clinical interview. There are many of these to choose from. The ones that we'll be discussing here are examples, but they're well validated. We'll also spend a bit of time talking about commercially available instruments that allow an individual to do a sleep study in the comfort of their home. We won't spend any time talking about polysomnography. That is a very specialized topic. But, of course, that is the gold standard for diagnosing all types of breathing problems that may be interfering with an individual's sleep. Among individuals with a substance use disorder, the clinician can conduct a focused clinical evaluation on their sleep in just a few minutes' time. That examination should focus on certain discrete areas, such as the onset of the problem, how long it's lasted, and any problems or impairment that have resulted from it. The clinician should inquire about whether or not the sleep problem is one of initiation or maintenance of sleep or both. It can also be quite illuminating to learn about the individual's dreams, presence of nightmares, and definitely whether or not they snore. Gathering as much information as you can about the person's sleep routine is very important. A bed partner can provide collateral history that may help understand whether or not the individual has some of the core symptoms of sleep apnea. And, of course, the medical history can be very pertinent, particularly such issues as pain. And finally, a person's medication history. Many, many medications interfere with the sleep cycle, and this will be an important point to consider in your assessment. So let's zoom in a bit and look at some specific questions that you may want to ask your patient about their sleep. You want to know what time they went to bed and what time they awakened for the day. It's also useful to figure out what awakened the individual, whether or not it was natural or whether or not they were abruptly awakened by an alarm. You want to get an estimate of how long it takes to fall asleep. For the normal individual, this ranges between 15 to 20 minutes. After falling asleep, you'd be interested in knowing how many times the individual awakened, what awakened them, would also be an important subset. It's also important to know how the individual feels once they awaken for the day. Are they tired, groggy, or refreshed? And you want to ask the individual, has anyone commented on your sleeping? This is a way to get at some information from a bed partner. And here you'd be interested in knowing whether or not the individual snores, complains of morning headaches, a dry mouth, a sore jaw, talking while they're asleep, walking in their sleep, or having jerking limb movements. Self-administered sleep-related screening instruments can be an important supplement to your clinical interview. There are a wide variety of these test instruments that are available. We're going to be discussing four. These are not exclusive, but they are validated instruments that can provide important information that will help you more fully understand the sleep problems that your patient is experiencing. We'll begin our discussion with the Pittsburgh Insomnia Rating Scale, followed by the Briefer Insomnia Severity Index, the Epworth Sleepiness Scale, and finally the Pre-Sleep Arousal Scale. The first instrument we'll look at is the well-validated Pittsburgh Insomnia Rating Scale, otherwise known by its acronym, PIRS. There are two versions of this instrument, this being the short version. There is a longer version, but this should suffice for screening purposes as a supplement to your clinical interview. As the name PIRS-20 indicates, there are 20 questions on the instrument that provides a fairly comprehensive insight into the factors that may be causing insomnia in your patients. Scoring is also fairly straightforward. Simply add up the scores that the patients indicated on the instrument. A score of 21 or above indicates the likelihood that the individual is suffering from insomnia. Next up for your consideration is the Insomnia Severity Index, otherwise known as the ISI. The ISI is a brief screening instrument that has an adequate internal consistency and is reliable in detecting changes after starting any treatment. As with any of these screening instruments, their utility can be extended not only to the initial detection of a sleep disorder, but also in monitoring any changes that your treatment may have. The ISI is a very simple instrument. It's only going to take your patients a few minutes to fill this out. Scoring is very simple. You simply add up the numbers that the patient has circled as their response to the seven questions. A score of 0 to 7 would indicate that there is no clinically significant insomnia present. A score of 8 to 14 is subthreshold insomnia. 15 to 21 is clinically significant insomnia of a moderate severity. And 22 to 28 indicates the presence of a severe insomnia. So the scoring basically goes in multiples of seven, which makes it easy to remember how to score this instrument. The Epworth Sleepiness Scale is often equated with screening for one of the key symptoms of obstructive sleep apnea, namely the daytime sleepiness or fatigue that accompanies that particular disorder. However, it's important to note that the Epworth Sleepiness Scale can measure the consequences of any impairment in the sleep that would cause daytime sedation. So it's not just used for screening for obstructive sleep apnea. Depression, for example, may also result in high scores on this instrument. So the Epworth Sleepiness Scale basically is assessing the chances that an individual may doze off in eight common situations, such as watching television, or as a passenger in a car, or sitting quietly after lunch, and that goes with the caveat without the use of alcohol. Now, scoring of this instrument is a bit more complicated, only in the sense that you need to remember a certain range of scores. Between six to ten, if the patient scores in that range, that's considered high normal daytime sleepiness. And the higher the score is within that range, the more intense your clinical focus should be in terms of perhaps expanding your clinical interview. If the patient scores 11 to 12, that would tend to indicate mild excessive daytime sleepiness. A score of 13 to 15 would be moderate excessive daytime sleepiness, and a score of 16 to 24 on the instrument would indicate the presence of severe excessive daytime sleepiness. The last screening tool we're going to explore is the Presleep Arousal Scale. This is an interesting testing instrument that can tell us several things about our patients. As you can see by looking at this slide, there are 16 questions. The purpose for this particular scale is to get some idea about what are the factors that are interfering with the patient's ability to fall asleep, in other words, what is inhibiting the initiation of sleep. So as you can see, it's going to take a little bit longer for the patient to fill this particular instrument out, but its value lies in getting a better grasp on the factors that are interfering with their sleep initiation. There are two ways to score this particular instrument. You can score all 16 items, just simply add up the numbers and you'll come up with a total composite score. But the real value of this instrument is the fact that it can be divided into two parts, and that is the purpose for the red line on this slide. The first eight questions are assessing cognitive factors that may be interfering with the person's sleep, such as worrying about falling asleep or perhaps reviewing depressive thoughts of the day, or they simply can't shut off an overly active mind. The second half of the instrument, questions nine through 16, are asking more somatic factors that may be interfering with sleep initiation, such as the individual feeling short of breath, or they feel tight and tense in their muscles. There is no cutoff score for the pre-sleep arousal scale. You'll simply look at this. The higher the number, the more significant that particular factor being cognitive or somatic is in interfering with their sleep. Home sleep studies offer a significant advancement in the opportunity to gather objective information about an individual's sleep. Home sleep machines basically expand an actigraph with physiologic measures and usually proprietary software that can then interpret a range of data that's generated through the overnight sleep study. Commercially, there are a number of these instruments that are available. Their sophistication is increasing as the technology also becomes more sophisticated. Home sleep studies offer a number of advantages. They can be conducted in the individual's natural environment in their bed with their bed partner, if they have one. They're less expensive than polysomnography, although, again, polysomnography remains the gold standard for diagnosing all types of sleep disorders. But home sleep studies are medically reimbursable. The CPT code 95800 is used for machines that are capable of reporting throughout the night on the individual's heart rate, their oxygen saturation, they can perform a respiratory analysis. They do this by airflow or peripheral arterial tone. And most importantly, they can calculate the amount of time the individual actually slept. CPT code 95806 can produce much of the same information, but lacks the ability to calculate an accurate time of sleep. So again, a home sleep study is an alternative to polysomnography in those situations where a degree of objectivity is required, and it may be a prelude to a more formal in-house inpatient diagnostic sleep study. This slide demonstrates the type of information that can be produced by a home sleep study machine. Look at the bottom of the slide with the red rectangle highlighting the graph. This particular sleep study machine is capable of identifying the stages of sleep that this individual went through. We can see when the individual was awake, when they were in light sleep, when they were in deep sleep, and when they were in REM sleep. We can also calculate how long it took the individual to fall asleep. We can see at what stage of the sleep cycle the individual awakened in. This particular machine also calculates an apnea hypopnea index. So home sleep study units can provide a wealth of information. And when used in conjunction with a sleep lab, can provide your patients with a great deal of specificity that may help them eventually and finally get that good night's sleep that they've been yearning for. So now let's pivot towards management of the sleep problems that we've detected through our clinical interview and the use of our screening instruments, and possibly also through the data gathered from a home sleep study. Of course, your first consideration should always be consultation. If the significance of the sleep problem warrants it in your clinical opinion, consultation with an individual who is an expert in managing sleep problems should always be considered. The second area that we're going to explore, albeit briefly, are the use of medications. Medications are a two-edged sword, and we'll explain that as we delve into that particular area. We're going to focus a bit more on suggesting some non-pharmacologic approaches to the management of sleep problems. These are behavioral approaches that are evidence-based and can be highly effective in helping your patient get a good night's sleep. We'll also focus on some very specific non-pharmacologic techniques, such as the use of cranial electric stimulation and acupuncture. In this particular case, we'll focus solely on ear acupuncture. When it comes to considering medications for sleep, there really is no perfect choice. This is probably particularly true among individuals that have a substance use disorder, since we have to take into account any addictive qualities that the sleep medication may have. In addition, we have to balance the effects on the sleep cycle. Most sleep medications are designed to help the individual decrease the time to sleep onset. However, once the individual falls asleep, the medication can have a number of adverse effects on the sleep cycle itself, leaving the individual unrefreshed and unsatisfied when they awaken the next day. We'll go into this in more detail in the next few slides. But as always, any medication choice is based on an individual assessment. Take into account all of the other medications the individual is taking and their medical condition and in the presence of any substance use disorder that may also be complicating the clinical picture. Take a moment to study this slide and the one that follows. What this chart demonstrates is the effect of a number of medications on the sleep cycle. And as you can see, most of the agents that are commonly used to help an individual with insomnia have profound effects on the sleep cycle. Usually these are directed towards decreasing REM sleep. Of course, individuals with depression commonly have problems with their sleep. And this may be one of the primary concerns that brings them into your office. And so certainly the use or consideration of an antidepressant is justified in individuals that may have a clinically significant depressive disorder. But as you can once again see, the antidepressants also have significant effects on the sleep cycle. And once again, it appears that most of these effects are directed towards increasing the amount of time when the first REM episode occurs and decreasing overall REM sleep. Now you can imagine if one starts combining sleeping medications with antidepressants that these particular effects can be compounded. Again, with the caveat that all medication choices have to be tailored towards the individual, one suggestion to consider, particularly for individuals that are clinically depressed and perhaps also among individuals that have a substance use disorder, would be to consider the use of Trazodone. Trazodone has interesting neuropharmacologic properties. It is a serotonin 2 receptor antagonist and a weak serotonin reuptake inhibitor. Serotonin 2 receptor antagonists have been shown to decrease sleep onset latency and to also increase deep sleep. Trazodone increases total sleep time and reduces wakefulness during sleep. And perhaps its most interesting characteristic is that it appears to exert minimal effects in suppressing REM sleep. Listed here are some other medication options that you might want to consider after doing your clinical interview with an individual that has a substance use disorder. Consider Doxepin. It's a potent H1 antagonist in the three to six milligram dose range. Prazosin for individuals with nightmares, particularly those with PTSD. Remeltion is a melatonin 1 and 2 receptor agonist and may have a place in the treatment of your patients with sleep problems. And finally, Suvarexant. Suvarexant binds to the orexin 1 and 2 receptors and promotes sleep through this mechanism. The remainder of this presentation will offer non-pharmacologic options for the treatment of sleep disorders. And the first one we're going to consider is a worry journal. This is a very simple approach that you can use for your patients that you've identified through your pre-sleep arousal scale that have cognitive factors that are interfering with sleep initiation. It's a simple device. You simply have the individual before they go to sleep, identify all the things that they're worried about, and then propose a solution for each. Then set that aside on their bed stand and have a good night's sleep, having prepared a plan to deal with their worries. It's simple, but in some patients it can be an effective intervention. We're next going to interview some behavioral treatments that have an evidence basis for their implementation. We're going to talk about sleep hygiene, stimulus control, and sleep restriction. Among the three behavioral interventions that we'll be reviewing briefly, sleep hygiene has the least evidence base to support its use. Now having said that, we still want to implement it because there are occasions when we can educate patients about practices that they've adopted that can easily be rectified and help them get a good night's sleep. Among those would be such things as minimizing or eliminating any caffeine products, alcohol, or stimulus such as nicotine before they go to bed at night. They need to make sure their bedroom is properly ventilated. Ventilated in temperature. Room temperature is an important component in getting a good night's sleep. Cooler temperatures are much better than warmer temperatures in terms of getting a good night's sleep. For a similar reason, exercising just prior to going to bed can raise body temperature and make it more difficult to sleep. Naturally avoiding fluids just before you go to bed will minimize the disruptions that come from having to visit the bathroom. So again, least evidence base for sleep hygiene, but still it's an educational activity and it may help some patients overcome some of the practices they've adopted. Stimulus control is a well-researched behavioral treatment that can have a positive impact on helping an individual get a good night's sleep. The patient needs to adopt certain practices to make stimulus control work effectively. They should go to bed only when they are sleepy. Perhaps the most difficult thing to do is if the individual is not asleep in 15 minutes, they need to leave the bedroom, go to a different area, engage in some non-stimulating activity, and when they feel drowsy, return to the bedroom. In an effort to reacquaint behaviorally the bed with sleep, the bedroom should only be used for sleep and sex. It's very important as part of stimulus control that the individual awaken at the same time every day, notwithstanding what time they went to bed. Stimulus control also requires that the individual not make up for their daytime sleepiness by taking naps. Patients that can engage in all the components of stimulus control and do it consistently will find that their sleep improves. Sleep restriction is another evidence-based behavioral treatment for insomnia. Before we discuss briefly how sleep restriction is implemented, we need to understand what sleep efficiency is. Sleep efficiency is a term that divides the ratio of time spent asleep to the amount of time actually spent in bed. For example, if a person spends eight hours in bed but only sleeps four of those hours, their sleep efficiency would only be 50%. The goal of sleep restriction is to achieve sleep efficiencies of between 85% to 90%, which means that only 10% to 15% of the time is spent staying awake in bed. So how do you achieve that? The purpose of sleep restriction is to introduce a mild sleep deprivation. The way it works is if the individual does not have the sleep efficiency that we just discussed, they need to adjust the time they go to bed. So say, for example, the individual typically goes to bed at 10 o'clock, but their sleep efficiency is only 50%. Have the individual go to bed 30 minutes later. They must get up at the same time, though, and then determine their sleep efficiency. This can be done with a sleep diary where the individual records the time they went to bed and the time they awakened and estimates the amount of time they were awake. If the 30-minute delay in the bedtime does not work, then it goes to sleep. Delay in the bedtime does not work, then it goes an hour. So instead of 1030 to 11 o'clock. And again, they get up at the same time. There will eventually be a set time during which the individual falls to sleep very quickly, within that 15 to 20 minute time period, and their sleep efficiency will steadily improve as the mild sleep deprivation. Kicks in. Now, obviously, this requires some effort on the patient's part. They must be motivated. And while this can be very effective, it does require that the patient stick with it. There are a variety of non-behavioral treatment interventions and certainly non-pharmacologic treatment interventions that clinicians can use to help their patients get a good night's sleep. Exercising on a regular basis earlier in the day, maintaining a healthy diet, healthy weight. These can all be beneficial. But here we're going to talk about some other options. One of which to consider would be the use of cranial electric stimulation. These are commercially available devices that deliver microamperage currents and can be very beneficial in some individuals in helping promote a good night's sleep. Although the way they work is not well understood, one thought is that they increase alpha-wave activity, which as we had previously discussed is a predicate to brainwave activity associated with the early stages of the sleep cycle. Another option that your patient and you might consider is the use of acupuncture. This particular slide shows what ear acupuncture looks like. There are five sites into which are inserted the needles in both ears. Exactly how acupuncture works is still a subject of research, not fully understood. It may have to do with relieving discomfort or pain. It may also promote general relaxation. Osteopathic manipulation is another viable option, particularly given a patient's interest in a non-pharmacologic approach or among individuals that have a substance use disorder where the use of medications may not be the best alternative. The possible treatment options that can be used include a suboccipital release, cranial osteopathic manipulative medicine, or rib raising. We've come to the end of this presentation on sleep problems associated with substance use disorders. I'd like to thank you for your attention and I hope you found this useful. So let's briefly review what we discussed. We talked about the normal sleep cycle. We talked about alcohol as the prototype for other sedatives, how it affects the sleep. We looked at the general principles of obstructive sleep apnea. And more particularly, we zoomed in on how alcohol and tobacco can contribute to breathing problems while asleep. And then we turned our attention to some clinical issues. In terms of how we can conduct focused sleep clinical interviews, the use of screening tools to supplement our clinical interviews, home sleep machines to provide more objective data. And finally, we looked at how we can manage some of these sleep problems, both pharmacologically and non-pharmacologically. Again, on behalf of the American Osteopathic Academy of Addiction Medicine, I thank you for participating in this slide set and I hope you found it useful.

Sleep Problems Complicated by Substance Use Disorders

Dr. Gregory Landy

The Essentials of Addiction Medicine

American Osteopathic Academy of Addiction Medicine

normal sleep cycle

alcohol and sleep

sedative drugs

obstructive sleep apnea

sleep-wake cycle

non-pharmacologic approaches to sleep problems