Key Points in the Diagnosis and Management of Mood Disorders Transcript PDF

Key Points in the Diagnosis and Management of Mood Disorders Transcript https://alt-5c5afaf83f339.blackboard.com/bbcswebdav/pid-2533770-dt-... Key Points in the Diagnosis and Management of Mood Disorders Well, welcome to week 2. And this week, we're goin...

Key Points in the Diagnosis and Management of Mood Disorders Transcript https://alt-5c5afaf83f339.blackboard.com/bbcswebdav/pid-2533770-dt-... Key Points in the Diagnosis and Management of Mood Disorders Well, welcome to week 2. And this week, we're going to talk about mood disorders and anxiety disorders. And in this slide set particularly, we're going to talk about key points in the diagnosis and management of mood disorders. So I realize I didn't introduce myself in week one. I expect that we've met in Nursing 6026, but if we didn't or, I don't know, for whatever reason, you just don't remember, my name is Sally Miller, and I am the professor that will be working with you for all of the psych-mental-health-speci!c courses. So anyway, we're going to talk in this slide set about key points, and I like that title because this isn't meant to be a comprehensive be all, end all. These are the highlights. This is the framework. And then you use the additional learning activities, the external links, your discussion boards, et cetera, to !ll in that gap and explore particulars of each item that I present here. So here we do have about 45 minutes or 50 minutes, for those of you that watch closely, worth of slide to point out the highlights and that it is my hope that between your books, your reading, your external links, your clinical experiences, you will round all this out to have a good handle, at least from a starting point, in the assessment and management of mood disorders. So with that said, we're going to go on to the topic at hand. Now, some of this may be a bit of a repeat from 6026. Truth is, I honestly don't remember exactly, but if it is, it's OK. Many of these concepts, you do need to hear them a couple of times before they really sink in. So if it's a repeat, forgive me. It probably won't hurt you. And if it's not a repeat, well, good. Here we're !nally talking about it. So given that our topic is key points in the diagnosis and management of mood disorders, one of the things that we do need to revisit is the physiology of mood disorders. Of course, mood disorders, like almost everything in mental health, are multimodal in their etiology, so there's typically a biologic component and a non- 1 of 18 11/2/24, 2:58 PM Key Points in the Diagnosis and Management of Mood Disorders Transcript https://alt-5c5afaf83f339.blackboard.com/bbcswebdav/pid-2533770-dt-... biologic component in just about everything. So best practices with respect to treatment will frequently include targeting the biological component and then targeting the non-biological component. So multimodal etiology is multimodal treatment. But in this discussion, and this semester for that matter, we really are focusing primarily on the biologic piece and applying the principles of pharmacology that we had in 6026, so hence the potential for overlap. But I do promise you, in another semester, we will focus exclusively on the nonpharmacologic management and the therapeutic interventions. I do always feel compelled to emphasize that even though the psych mental health nurse practitioner largely is a prescriber-- I mean, that is primarily how we treat illness, unless you really focus on the therapeutic modality-- but even those of us whose practice primarily is about prescribing, we always need to acknowledge the nonpharmacologic component necessary in disease management. So more about that to follow, but for right now, key points in the diagnosis or assessment and diagnosis and management, whatever, of mood disorders, we're going to take a look at the biology speci!cally and synaptic transmission. Synaptic transmission is the target of virtually all pharmacotherapy in the world of mood disorders. So you know what a synapse is. I'm sure we've talked about it in other courses, or you've talked about it in another course somewhere. The synapse is the connection between two or more cells. We are interested in neurons, obviously, in the central nervous system, so we will refer to synapse as that specialized region of contact between two neurons, and it's where communication from one cell to the others occurs. Synaptic transmission can be either electrically mediated or chemically mediated. Electrical synapses are when the cell membranes of the two cells and communication are actually touching each other, and so it's electricity that moves from neuron to neuron that communicates the message. When you don't have the two cell membranes in direct contact, you need a chemical transmitter to di"use across the synaptic cleft to carry the message from one neuron to the other, from the presynaptic neuron to the postsynaptic neuron. This is especially relevant in mood disorders because the physiology of mood disorders, at least some of them, is fairly well-de!ned, and for whatever reason, and that reason really is not entirely clear, but for whatever reason, when there is an imbalance or dysregulation of certain neurotransmitter concentrations in speci!c neural pathways, then we wind up with a mood disorder. I do feel compelled to point out to you right now that this has been the theory of the 2 of 18 11/2/24, 2:58 PM Key Points in the Diagnosis and Management of Mood Disorders Transcript https://alt-5c5afaf83f339.blackboard.com/bbcswebdav/pid-2533770-dt-... etiology of depression. Depression is pretty well-articulated in the mental health literature. The physiology of mania, or elevated mood, is not as well-de!ned. There's a theoretical construct, and we'll talk about that in a little bit. But the physiology of depression has, for decades now, really been-- we have considered that it is well- de!ned. We might not know why it happens, but we have accepted that depression occurs when there is an imbalance of certain neurotransmitters in certain pathways, and virtually every pharmacologic agent to treat depression targets those neurotransmitters and those pathways. It just so happens that literally, in the last couple of weeks, a study came out of-- I want to say the Netherlands, somewhere in that part of the world, which is where a lot of good science originates. A study came out that basically said, it's all not true, that the whole neurotransmitter theory of depression is just a big lie. So, obviously, it is one study. It is going to take a whole lot more. I didn't read the whole thing, but I just skimmed through it, going, oh, my gosh. OK, this is sort of a thing in the world of mental health. Anyway, it is the beginning of a conversation, that over many, many years, there will be studies that are more re!ned, better controls, and we'll see what that's all about. There is absolutely no denying that when we correct neurotransmitter balance in certain patients, their mood improves a lot. But maybe it's for some other reason that nobody has identi!ed yet, so I'll see if I can make that article available to you, at the very least, when I can make the link available to you so that you can read about it. It's an interesting thought, but I do want to emphasize, for right now, we're not going there. It takes more than one study to completely reorient our whole therapeutic approach in psychiatry. So for right now, we will continue to regard the etiology and treatment of depression as we always have, but I just wanted you to know that somebody has just thrown the !rst initial little wrench in that line of thought. And as your career progresses-- I'm sure I'll be long retired-- but as your career progresses we may come up with a whole new etiology of depressed mood. But right now, it's really about chemical transmitters and synapses. So by way of reminder, I'm sure you've seen something like this before. We have a presynaptic neuron and a postsynaptic neuron. Let me see if I can get my laser pointer here. There we go. OK, so we've got a presynaptic neuron and the postsynaptic neuron. And the presynaptic neuron contains neurotransmitter that's collected in little vesicles, and when a stimulus occurs, those vesicles will fuse with the inner surface of the neuronal membrane and release neurotransmitter into the synaptic cleft, which is that 3 of 18 11/2/24, 2:58 PM Key Points in the Diagnosis and Management of Mood Disorders Transcript https://alt-5c5afaf83f339.blackboard.com/bbcswebdav/pid-2533770-dt-... extracellular space between two neurons. And then that neurotransmitter will bind to postsynaptic receptors and e"ect some sort of message in the postsynaptic cell. And in the world of mood disorders, there are particular neurotransmitters that we have come to recognize as being implicit in changes of mood. So this is what a chemical synapse looks like. Neurotransmitter is our treatment target in the world of mental health disorders. OK, so synaptic transmission involves four processes, and they are listed here. And I list them only because this is what we target with drug therapy. Synaptic transmission involves four distinct processes: release of chemical transmitter from the presynaptic neuron, di"usion across the membrane, binding to the postsynaptic receptor, and then inactivation of transmitter. This is an important one down here at the bottom. We do have to eventually inactivate that transmitter because we can't have too much of its activity going on for too long, or you will have an exaggerated response to it. That's not going to be a good plan either. So these are the four steps. And, actually, when it comes to drug therapy, what we really are targeting primarily is number one, number three, and number four. Di"usion of transmitter to the postsynaptic membrane, it's such a quick process, and there's really not much that we can do about that. But various drug therapies, one way or another, will target number one, three, or four of these steps. So I know I got a little bit carried away here, and I know we talked about this in another course. But, by way of reminder, depolarization is when the voltage in the presynaptic neuron goes up. Remember that resting voltage, or resting potential voltage, in any neuron, there's a resting state and then an active state. In the resting state of neurons-- [coughs] --excuse me, the voltage is somewhere around minus 60 or minus 70 millivolts. A depolarizing stimulus is a thing that raises the voltage from minus 70, minus 60, minus 50, minus 40, minus 30, minus 20, et cetera. When a neuron is depolarized, when the voltage rises to threshold, well, then an action potential occurs. It's an all-or-nothing. Once the neuron reaches threshold, well, then this response is going to happen, and that's when neurotransmitter is released. And so the neurotransmitters of interest with respect to mood disorders are right here. Serotonin, norepinephrine, dopamine, glutamate, these are the primary neurotransmitters implicit in mood disorders. So if we have a patient with an abnormal 4 of 18 11/2/24, 2:58 PM Key Points in the Diagnosis and Management of Mood Disorders Transcript https://alt-5c5afaf83f339.blackboard.com/bbcswebdav/pid-2533770-dt-... mood, there is likely an abnormality in the concentration of one or more of those neurotransmitters in certain neural pathways, and our drug therapy is targeted to trying to correct it. Here's just another way of looking at it. I know you've seen this before, so I will step it up here a little bit. Another example-- presynaptic neuron. This one contains dopamine. When this neuron is depolarized to threshold, it will release dopamine, the dopamine di"uses across the synaptic cleft and binds to postsynaptic neuronal receptors and will produce some sort of response in this postsynaptic neuron. And then dopamine needs to be inactivated. We don't want it hanging around too long, or we will have an exaggerated response to it. So dopamine is inactivated in several ways, but one of them is that it is pumped back into the presynaptic neuron. It is reuptaken by the presynaptic neuron. And this particular slide is showing you that when people use cocaine, the way cocaine makes you euphoric is by blocking those presynaptic neurons, so dopamine can't be pumped back into the presynaptic neuron, which means it hangs around here at the synapse longer, which means there is increased dopamine intensity. And dopamine in certain areas of the brain is the feel-good neurotransmitter. So we want to feel a little good, but we don't want to feel too good. That's like high or euphoric or psychotic, depending on which part of the brain we're talking about, which is why cocaine can do all those things to you. If you block reuptake and increase dopamine concentration in certain neural pathways, you will just have exaggerated euphoria. If you block dopamine reuptake and have exaggerated dopamine e"ect in other areas of the brain, you will have psychoses. Neither of them a good plan. So transmitter has to be inactivated, and it's important. And the reason I'm highlighting it here is because this is a common target of pharmacotherapy for mood disorders. So, like I said, once the neurotransmitter has done its job, it needs to be inactivated, and there are three primary mechanisms by which neurotransmitter is inactivated. One is that it's just the law of di"usion. First law of di"usion, solutes will move from an area of high concentration to an area of low concentration. So because you dump a bunch of neurotransmitter in the synapse, it will just di"use away into the extracellular space. So that's good. Another way that we get rid of neurotransmitter is to degrade it by way of enzymes. Neurotransmitters are just chemicals, and chemicals are created by a series of elements bonded together. And anything that's bonded can be debonded, right? Bonds can be broken. 5 of 18 11/2/24, 2:58 PM Key Points in the Diagnosis and Management of Mood Disorders Transcript https://alt-5c5afaf83f339.blackboard.com/bbcswebdav/pid-2533770-dt-... And enzymes accelerate the breaking of those bonds and break down the transmitters into component parts. And there are several enzymes that are targets of pharmacotherapy. And then, !nally, like the example I just showed you, sometimes we inactivate transmitter by pumping it back into the presynaptic neuron. So these are all normal processes that in the healthy patient with no abnormalities controls the amount of neurotransmitter so that you have just the amount that you need. In patients with mood disorders, either we have too much neurotransmitter or too little neurotransmitter in certain pathways, and we try to correct that imbalance, and inactivating transmitter is among the ways that we can do it. So another picture paints a thousand words, right? We're still talking about dopamine here. So you have the concept, presynaptic neuron releases dopamine. Dopamine di"uses across the synaptic cleft and binds to transmitters, or, rather, binds to postsynaptic receptors. So that's great. But then in order to get rid of it, we've already seen that there are reuptake transporters. Another way that we get rid of dopamine is enzymatic degradation. "COMT" is "catechol-O-methyltransferase," and "MAO" is "monoamine oxidase." These are two naturally occurring enzymes that degrade dopamine. And so in circumstances where we want to increase the concentration of dopamine, we could block a reuptake transporter, or we could block enzymatic degradation. And you know that we have medications that are COMT inhibitors, and we have medications that are MAO inhibitors. And I know you know that because you took 6026, and I'm sure you remember everything we talked about in that course. Just another neurotransmitter giving you the same example. Presynaptic neuron, neurotransmitter, reuptake. And, of course, blocking reuptake of serotonin by way of selective serotonin reuptake inhibitors is very famous. So that is the treatment target. Now you'll notice that I'm concentrating here more on depression than I am on mania, and it's because the physiology of depression is much better understood. The physiology of mania is not especially well-understood, but we'll talk about that in just a moment. Now, neurotransmitter is the !rst concept of interest. The second concept of interest is the pathway. With all the mental health disorders, we're talking about a handful of neurotransmitters, and di"erent disorders occur when there are imbalances of one or more of these neurotransmitters in di"erent pathways. And so in major depressive disorder, the two pathways that have been best 6 of 18 11/2/24, 2:58 PM Key Points in the Diagnosis and Management of Mood Disorders Transcript https://alt-5c5afaf83f339.blackboard.com/bbcswebdav/pid-2533770-dt-... articulated-- and, of course, there are others-- but the two that are best de!ned and best articulated are the raphe nucleus and the locus coeruleus. These are both part of the reticular activating system, which is the system, really, that controls arousal. The reticular formation is the part of the brain, and the RAS is part of that. That's the part of the brain that controls various levels of arousal. From sleep to wakefulness, to hyper arousal, to sexual arousal, to the increased arousal that occurs when you are having an anxiety reaction, this all occurs in the reticular formation and their reticular activating system. And what has been observed for many decades now is that when there is decreased neurotransmitter function in those two pathways, it correlates to depressed mood, and when we give medication that increases the concentration of neurotransmitter in those pathways, this correlates to improved mood. Like I said, this is the theory that this researcher out of the Netherlands is saying is all a lie, but I'm editorializing. I guess she didn't quite say it's a lie, but she basically said the serotonergic theory of depression just doesn't hold water when they investigate it. So it's something we all need to read. I need to take a deeper dive into it, and you should at least be introduced to the idea that there are researchers now that are questioning this hypothesis. But anyway, like I said, for the last, I don't know, 50 years and right now, we still consider this the primary biologic modality of depressed mood. And so here's where they are. I know it's an old-fashioned looking picture, but it's just the best one I have with just the level of detail that I like to present here. So here is the pons. Right? This is part of the reticular formation. And the area of interest, we-- I was going to say "me and my personalities"-- I've circled and blown up over here, and you see it contains the locus coeruleus and the raphe nucleus. And you see the neurotransmitters that are most prevalent in that areas. And, for whatever reason, we do know that people that have depressed mood often have corollary low levels of neurotransmitter activity in these areas, and when we produce a biologic response that increases neurotransmitter in those areas, mood improves. So if the mechanism by which that happens is the thing that's wrong, who knows? News to follow on that one. But for right now, our primary treatment targets of depressive therapy are these areas of the brain. So that's depression. Like I said, depression is fairly well-understood. There's more to it than that. We're not doing a deep dive into the neurophysiology of mood as our entire degree here, and I don't claim to be an expert on it. But this is a commonly held tenet in mental health. It is pretty well-articulated. 7 of 18 11/2/24, 2:58 PM Key Points in the Diagnosis and Management of Mood Disorders Transcript https://alt-5c5afaf83f339.blackboard.com/bbcswebdav/pid-2533770-dt-... The other end of mood? Not so much so. So the other mood disorders that we need to consider are those that include elevated mood-- some degree of mania, hypomania. That's part of the bipolar discussion, right? Bipolar disorder is a disorder that's characterized by two poles, two extremes of mood-- the patient who has depressive states and the patient who has either a manic or hypomanic states. And as well as we think we understand the physiology of depression, that's how well we don't really understand the physiology of mania. It is not a well-understood construct. But there are lots of theories, and we do know that there are certain medications that can help control mania and level the patient's mood out. So it de!nitely is a theory at this point. There's lots of work to do in supporting it. But for right now, our understanding of the physiology of mania is that there are numerous pathways both in subcortical structures and prefrontal cortex structures that are theorized to contribute to the symptoms of elevated mood. There are numerous pathways, and that's purported to help explain why there are so many potential symptoms of mania and why people can experience mania very di"erently. I mean depression, this is also true enough. Some people are depressed, and they're sad all the time. They'll tell you they feel depressed. Other people meet diagnostic criteria for depression, but they'll tell you they're not really depressed. They don't feel sad. They don't feel depressed. They just have no energy, no interest. Other people that have a diagnosis of depressive disorder have real issues with sleep or appetite. Some patients don't. Other patients that have a diagnosis of depression really are consumed by a sense of worthlessness, hopelessness, and others, not so much so. So even with depression, we can see that there are di"erences in symptom presentation, but there are some core features that are always there. Like a patient with depression will either have depressed mood or a sense of anhedonia. Right? Not looking forward to anything, not being excited by anything, not being motivated. And then other symptoms will vary a bit. So clearly, there are some issues there in pathways that we don't fully understand. But with mania, you can have !ve di"erent patients having a manic episode, and their symptoms are really di"erent. Some people have that true stereotypical grandiosity. They can do anything. Everything is wonderful. Everything is amazing. They're euphoric. Some people with mania are so euphoric, they hallucinate. Other people, it's not so much this sense of euphoria as this profound sense of drive 8 of 18 11/2/24, 2:58 PM Key Points in the Diagnosis and Management of Mood Disorders Transcript https://alt-5c5afaf83f339.blackboard.com/bbcswebdav/pid-2533770-dt-... and purpose. They get stu" done. Lots of creatives are most creative in a manic or hypomanic state. People that are like writers and musicians and songwriters and actors, actresses, all that kind of stu", they're most creative when they are in a manic or hypomanic state. Then we have other people whose mania is characterized, really, by profoundly inappropriate behavior, by what we would say "no !lter." They just say whatever comes to mind even if it's totally inappropriate, or do inappropriate things. It looks like they just don't even have any sense of social folkways or morays. Other people's mania is largely characterized by disproportionate anger and irritability and disproportionate responses, and so it makes sense that there are probably numerous prefrontal and subcortical pathways that are involved here, because the pathways involved are what helps produce the symptoms that the patient is experiencing. So just by way of example, these are some of the neural centers that are believed to be a"ected in the patient with elevated mood. We have, well, down there at the bottom, the amygdala. We'll talk a lot more about the amygdala when we talk about anxiety. Amygdala is, really, command central for the fear response. A patient with a healthy amygdala will experience fear when something fear-inducing happens. They'll experience anxiety when something anxiety-inducing happens. If they're #ying in an airplane, and the thing starts diving around or bouncing around, there's a storm, and it's a bad #ight, they'll start to get a little apprehensive and tachycardic and a little tachypneic and hypervigilant, because that's normal, right? The amygdala perceives sensory input and then generates that appropriate anxiety or fear response. And, of course, if the amygdala is not working quite right, if there's dysfunction in those pathways, you may either have the inability to experience fear, which we see in manic episodes, or the anxious patient will have an excess of amygdala responses. So in patients who are manic, it may be that they are having disorder in amygdala pathways, and they just don't experience normal levels of fear or apprehension. The anterior cingulate cortex. We have a dorsal and a ventral here, the ACCs. The cingulate cortex, really, has a role in mood regulation, attention allocation. You attend to something appropriately, whereas people with manic episodes sometimes don't attend to things appropriately or may pay too much attention to something inappropriately. 9 of 18 11/2/24, 2:58 PM Key Points in the Diagnosis and Management of Mood Disorders Transcript https://alt-5c5afaf83f339.blackboard.com/bbcswebdav/pid-2533770-dt-... The cingulate cortex cortices also have a role in emotional expression, how you respond to a stimulus. We know that in day-to-day life, things happen, and there are certain appropriate emotional responses to it. And those are regulated by the cingulate cortices. The dorsomedial prefrontal cortex that you see up here, this is attributed with the coordination between cognitive and emotional function. You know, cognitive being your thought processes, executive function, how you process information, and the emotion obviously is, well, how you respond to it. And so, again, having an appropriate emotional response to appropriate cognitive stimuli, that's balanced by the dorsal medial prefrontal cortex. Whereas the dorsolateral prefrontal cortex, this one is really more linked to higher-order cognition, not so much emotion but higher-order cognitive function, like the ability to abstract appropriately, the ability to apply one thought process to other concepts, executive function, multitasking. The dorsolateral prefrontal cortex is also credited with the ability to inhibit inappropriate emotional responses. Like you may experience something, and you have a response. And that response might really be deep and heartfelt and strong, but it's not appropriate in that time or with that circumstance or interaction. And your DLPFC will protect you from it, whereas with the manic patient, not so much. The ventrolateral prefrontal cortex, this one is more linked to the emotional piece, like a sense of reward, the sense of motivation. The grandiosity that we see in some patients with manic symptoms may be attributed to abnormalities in the pathways there. So di"erent areas of the brain are linked to di"erent behaviors and di"erent skills, and so the current theory of elevated mood is that there may be abnormalities in any one or more of these pathways. This is just a slightly di"erent way of looking at it. It also brings the rest of the centers here into view, like the hypothalamus. I know it's here somewhere. I saw it. There we go. The hypothalamus. And I don't see the hippocampus labeled here, but it's right next to the hypothalamus. These are really important areas with respect to memory and memory processing, remote memory. Oh, there's the hippocampus. Yeah, I knew it here somewhere. The raphe nuclei and locus coeruleus, we already talked about that and how those are so implicit in depressed mood. And you can see when you look at it this way how a patient can have a mixed bipolar episode, how you can be both depressed and manic at the same time. They're di"erent pathways. The depressive mood is really more of an 10 of 18 11/2/24, 2:58 PM Key Points in the Diagnosis and Management of Mood Disorders Transcript https://alt-5c5afaf83f339.blackboard.com/bbcswebdav/pid-2533770-dt-... issue with dysfunction here. [clears throat] Excuse me. Manic episodes are more a consequence of dysfunction in pathways anywhere around here. And so, yes, people can have both depressed and manic phenomena at the same time because you can have disorder, dysregulation among several pathways. And then you also see the vagus nerve is in very close proximity, which no doubt has something to do with some of the physiologic responses that occur when we have abnormalities of mood. So, interesting. Not well-de!ned but at least enough that we can look at this, and then we can look at the drugs we use considering synaptic transmission and say, OK, the patient with depressed mood, there's not enough serotonin in the synapses in this area of the brain, so we give SSRIs to block inactivation, increase serotonin concentration, and improve mood, whereas in the patient who's having a manic episode, where they can't !lter their thoughts, or they don't attend appropriately, or they don't have appropriate perception of circumstances, then dysfunction may be in glutamate pathways. Or norepinephrine pathways appear somewhere, and we can try to normalize regulation with medications. So that's why we talk about this. And that, of course, is our foundation for how we manage mood disorders. One of the most important pieces of appropriate management of a mood disorder is actually recognizing the mood disorder and diagnosing it correctly. And I know I've talked about this before, too. I keep bringing up the same things because these are the mistakes that new clinicians often make. So before we even talk about treating a mood disorder, !rst we have to make sure we've actually made the right diagnosis. So in the world of mood disorders, we have an entire spectrum here. "Mood disorders" is a generic term. If you look in the DSM, there's a whole bunch of mood disorders that really describe any variety of abnormalities that occur within the spectrum of identi!ed mood. And, yes, keep in mind that it becomes a disorder when the symptom constellation, number one, meets diagnostic criteria, but also of equal importance, and even perhaps more important, is that the symptom or symptoms produce impairment of social and/or occupational function. Virtually every psychiatric diagnosis is characterized by some disorganization and social or occupational function. So here are the !ve commonly identi!ed levels of mood, and, again, I didn't make this up. This is the common approach to evaluating mood. And down here, at the very 11 of 18 11/2/24, 2:58 PM Key Points in the Diagnosis and Management of Mood Disorders Transcript https://alt-5c5afaf83f339.blackboard.com/bbcswebdav/pid-2533770-dt-... bottom, we have depression. And depression is classically de!ned. A depressive episode is classically de!ned as the patient having !ve of nine symptoms. You will have readings about it. Your DSM will make it very clear. There are nine domains, and patients need to have symptoms from a minimum of !ve of them. And that constitutes a depressive state or depressed mood. "Mania" is here at the very top of the mood spectrum, and there are diagnostic criteria for mania, too. And they include things-- and you can refer to your DSM for speci!cs-- but mania by de!nition, true mania typically is characterized by a period of sustained wakefulness of at least 40 hours duration. And not just that the patient's awake but that they don't feel the need to sleep. They are awake. They are hyperalert. They are active and usually very productive. And then there are other symptoms like grandiosity, easy distractibility. I'll refer you to your DSM for all the speci!cs. But to achieve each of these extremes of mood, there are criteria that need to be identi!ed. In between, we have dysthymia, euthymia, and hypomania. Dysthymia is the patient who has depressive symptoms, but they don't quite meet a major depressive episode. Maybe they don't have !ve out of nine, but they have two or three, enough that it's reducing social or occupational function. Also characteristic of dysthymia is chronicity. True depressive states, people will cycle in and out of them, but the dysthymic patient tends to go-- I think the diagnostic criteria for an adult is two years without an improvement of symptoms. Hypomania, the patient experiences many of the same symptoms of mania, although the prolonged wakefulness is not required, but just not to the extreme. One of the de!ning features usually of mania is that true mania often gets picked up when the patient comes to the attention of law enforcement. Because their judgment is so clouded and their actions are just so wrong that they wind up getting in trouble for it. The hypomanic patient, there's usually some disturbance of social or occupational function, but the elevated mood is not that extreme. And then, of course, euthymia is the normal state of being, the normal ups and downs that we all experience in day to day, and mood disorders are re#ected by some abnormality, some deviation from euthymia that, at a minimum, has the patient moving from dysthymic to hypomanic, et cetera. So these are the !ve levels of mood. And patients with a depressive episode or major depressive disorder will cycle between normal mood and depression. This is key. Patients with a diagnosis of major depressive 12 of 18 11/2/24, 2:58 PM Key Points in the Diagnosis and Management of Mood Disorders Transcript https://alt-5c5afaf83f339.blackboard.com/bbcswebdav/pid-2533770-dt-... disorder, they will have periods in between where they are not depressed. They cycle from, quote "normal" to diagnostic criteria for depression. Whereas the bipolar I patient, this is the patient that cycles between true mania and true depression. You will usually see them here unless a court orders them to be here or something, but usually they present when they are depressed. And, as I'm sure you remember from 6026, one of our most important pieces of working up somebody for depression is that we look into the history for a history of manic activity or manic symptoms because we de!nitely want to distinguish the patient who is depressed, where we cycle from euthymia to depression, versus bipolar I, where you cycle from mania to depression. Mania is fun for a lot of people, and they don't have a problem with it and don't see it as a problem and may not even mention it unless you ask speci!cally. Bipolar II is di"erent. The distinction between bipolar I and bipolar II is the di"erence between mania and hypomania. This is the one that's easiest to confuse with a major depressive episode. Unless we speci!cally explore the history for hypomanic symptoms, you might miss it because the patient, again, will usually present for care when they're down here. So if they're going from euthymia to depression, that's how you support your diagnosis of major depressive disorder. But if they have history of hypomanic episodes, then that's the bipolar II patient. And, as I'm sure you remember from Nursing 6026, the reason this is so important is because the treatment modalities are di"erent. And then we have patients who cycle up and down to the extent that it does interfere with social or occupational function. It's a problem in their world in some way. But they don't meet criteria for depressive episodes, and they don't meet criteria for manic episodes. And that's the patient who, more literally, is cyclothymic. You will often see them diagnosed as mood disorder not otherwise speci!ed. Right? The name just tells the story. They have a mood disorder, but the disorder doesn't meet criteria for mania or depression. So that's why we have to be really careful about how we use these diagnoses, how we throw them around. It is very often, people get assigned a diagnosis of bipolar disorder or even depression. They get hit up with one of these diagnoses, but when you explore the history, they genuinely don't really have any symptoms that are consistent with it. And they're not appropriately diagnosed, which might explain why they don't actually respond to treatment. So that's that. 13 of 18 11/2/24, 2:58 PM Key Points in the Diagnosis and Management of Mood Disorders Transcript https://alt-5c5afaf83f339.blackboard.com/bbcswebdav/pid-2533770-dt-... OK, so probably the next few slides just say everything I just said. Yup, they do. I got excited as usual and said it too fast, but, as always, I !rmly believe it never hurts to hear this stu" twice. So major depressive disorder? There you go. Cycle between euthymia and a depressive episode, typically presents as the classic !ve of nine, and, yes, these are the patients who best respond to antidepressants. And, of course, they also should be referred to a therapist. And, as I say, we'll talk more about that in another semester. Dysthymia is di"erent. Dysthymic patients may appear depressed, but if you actually do a diagnostic evaluation, you'll !nd that they don't really meet criteria for major depressive disorder. But they do have symptoms that are causing a depressed mood, and it's chronic. I think under the age of 18, diagnostic criteria is one year with no break in symptoms, and over the age of 18, two years with no break in symptoms. And the reason that it's important to identify the distinctions is, number one, we just want to make the right diagnosis. Just like you wouldn't diagnose somebody with hypertension without measuring two blood pressures, at least, on two separate occasions that were above 140 over 90. We don't diagnose depression unless the patient meets criteria. We diagnose dysthymia when the patient meets criteria. But, more importantly, these patients don't respond as well to antidepressants. These patients really are best referred to a therapist. Now, the mood disorders, the "up" mood piece of it, we talked a little bit about this, too. There is a mnemonic for elevated mood. It's called "DIG FAST." And I'm not going to remember what they stand for, but I'm sure it's in your readings somewhere. "D" is for "distractibility," "I" for "irritability," "G" for "grandiosity." DIG FAST. What does the "F" stand for? Mm-mm-mm. Oh, I don't know. A, I think, is "attention." "S" is "sleep," and then "T" is I don't know. So I got most of them. But anyway, there is a mnemonic for up mood, and these are the core features that are re#ected in that mnemonic. So I mentioned two or more sleepless nights. Now, again, these are diagnostic criteria, but you also have to use some clinical judgment here. Some people are so elevated that they do actually hallucinate. And, yes, another thing I think I didn't mention was the history of risk-taking behavior because they don't genuinely perceive it as a risk. There's that amygdala pathway dysfunction. Another characteristic very common to bipolar II is the binge behavior. Shopping, eating, whatever it is they do, they tend to do it too much. 14 of 18 11/2/24, 2:58 PM Key Points in the Diagnosis and Management of Mood Disorders Transcript https://alt-5c5afaf83f339.blackboard.com/bbcswebdav/pid-2533770-dt-... People that binge-shop will often tell you that they still have stu" in their closet, in bags, in boxes. They bought stu". They didn't even need it, but they just bought it because they were having fun. And then they put it away, and that was that. Binge gambling-- it doesn't take long to !gure out that gambling is a problem. And hypersexuality is also not uncommon in the patient with elevated mood. So, as I mentioned before, bipolar I is the most extreme of cycling. The di"erence between bipolar I and bipolar II is that instead of manic episodes, patients have hypomanic episodes. And then, yes, !nally cyclothymia, the artist also known as mood disorder not otherwise speci!ed. What's really signi!cant here is that they don't meet criteria for anything, but their cycling and mood is causing a problem of some sort. I mean, it's not like patients come in and say, hello, I appreciate that my cycling mood is a problem. Can I get help? That's not the way it goes. But maybe the signi!cant other says, listen, you just get so angry all the time. It's not normal. It's not right. I can't live with it. You have to go get some help. And then when you talk to the patient, you !nd out, yes, they have this temper, this irritability. It's causing a problem in their relationships, or it's causing a problem at work. Right? That is interfering with social and occupational function. Same thing with the depressive symptoms. The patient might say, I don't feel depressed. I don't feel worthless. I go to work. I'm doing what I need to do. I pay my bills. I'm taking care of business. But they still have symptoms of down mood that are a problem either at work or at home or at school or whatever. So that's your "not otherwise speci!ed." And, again, the distinction among these disorders is really important in terms of !nding appropriate treatment. It is not uncommon that you will see somebody referred to you by primary care because they're not responding to antidepressants, and then, lo and behold, you realize the reason they're not responding is because they don't have a diagnosis of depression. They're dysthymic. They need a therapist. Or they're not responding to antidepressants because they actually have bipolar II, and antidepressants are the worst thing for them. So appropriate diagnoses are important. So let's see. What does this say? Any patient who presents with depressive symptoms, yes, should be evaluated for a history of cycling. I know you've heard me say it before, and you'll hear me say it lots of times again because it is so important. If you don't remember anything else from this entire discussion, please, please remember that 15 of 18 11/2/24, 2:58 PM Key Points in the Diagnosis and Management of Mood Disorders Transcript https://alt-5c5afaf83f339.blackboard.com/bbcswebdav/pid-2533770-dt-... before you put a diagnosis on somebody's chart, you really want to assess for diagnostic criteria for that thing. And number two, before you assign a diagnosis of depression, you absolutely want to explore the history for elevated mood, mania or hypomania. Because if they do have histories of elevated mood, then they don't have a major depressive episode, and we don't treat them with an antidepressant. Antidepressants can actually make those patients worse. Sometimes that's how we !nd out they're bipolar, is primary care gave them an antidepressant, and they started bouncing o" the walls. And it's like, aha. Let's talk about this. And then you !nd out that they actually precipitated a manic or hypomanic episode. OK So, yes, I already talked about bullet point A. So once you do deduce that the patient is having a major depressive episode or the patient has major depressive disorder, then it is appropriate to manage them with your classic antidepressant medications. The SSRI-- I mean, all of these drugs, we did talk about them in 6026, so I won't perseverate over it here. If you don't remember, you can probably go back into that course or at least whatever notes you have from it and revisit it. But the depressive episodes, drug therapy is with an antidepressant. Of course, nondrug therapy is also a really important part of this, and we will explore that in 6972. But do keep in mind that true mood disorders usually are multimodal in their origin, and patients typically-- with rare exception-- patients have their best outcomes with a combination of both therapies, nonpharmacologic therapies, and drug therapies. Whereas bipolar I and bipolar II is not managed with antidepressants. Now, again, I know that you will sometimes see an antidepressant in the cocktail. Sometimes you do have to do that. Sometimes you get a really good handle on their mania. And in managing their mania, some depressive mood pops through, and then it might be appropriate in certain circumstances to add an antidepressant to it. But you would never want to take a patient with a diagnosis of bipolar I or II and have them on an antidepressant as monotherapy. Anybody with bipolar that needs medication needs to be on a mood stabilizer or an antipsychotic. So remember, also from 6026, that mood disorders, it's a little bit di"erent. It's not just, oh, everybody starts with an SSRI and then maybe go to an SNRI. In the world of mood disorders, because mood disorders are characterized by two poles, the elevated pole and the depressed pole, it really depends on when you're seeing the patient and what 16 of 18 11/2/24, 2:58 PM Key Points in the Diagnosis and Management of Mood Disorders Transcript https://alt-5c5afaf83f339.blackboard.com/bbcswebdav/pid-2533770-dt-... is the primary treatment target. We have manic-minded mood stabilizers. Remember, valproic acid, carbamazepine, and, of course, the prototype lithium. We have depressive-minded mood stabilizers like lamotrigine, which is really it. We have lots of antipsychotics now have indications for bipolar depression or all mood variations of bipolar disorder. And so the patient with a bipolar I or a bipolar II that needs pharmacotherapy, it is going to include, at a bare minimum, either an antipsychotic or a mood stabilizer. More often, it's going to include both. And for the patient with breakthrough depression, yes, sometimes we have to add that third class of medication to it. Whereas major depressive disorder can often be managed with one drug agent-- monotherapy. Patients with bipolar disorders usually have to be managed with polypharmacy. There is, of course, an exception to every rule, but the rule is depressive disorder, you can get away with one drug. Bipolar disorder, you can't. And so let's see. I think this is our wrap-up slide for this discussion. While the majority of patients who present to a mental health practice with mood-- easy for me to say. Let me say that one more time. This is what happens when your brain moves faster than your mouth. Let's try it again. While the majority of patients who present to a psych mental health practice with mood disorders will require pharmacotherapy, dot, dot, dot-- yes, the majority will need pharmacotherapy-- all patients who present to you with mood disorders should have non-pharmacotherapy. At a minimum, at a minimum, they should be referred to an appropriate type of therapist for nonpharmacologic intervention, and then, depending on the severity of symptoms, very often, with mood disorders, drug therapy will be appropriate. And I probably should even go on further to say here, when they !rst present to you, keep in mind that patients will often have symptoms for sometimes a very long time, and they self-medicate with alcohol or self-medicate with drugs, substances of abuse. Or they just try to handle it, or they can sometimes even adjust their life to accommodate it. And so sometimes patients go for a long time with symptoms of a mood disorder before seeking mental health care. And so it may be that by the time the patient makes the !rst appointment with you, they're at their worst of the worst. Their depression is at its lowest low, or their mania got him arrested. Right? And that may not be the time for a therapist. 17 of 18 11/2/24, 2:58 PM Key Points in the Diagnosis and Management of Mood Disorders Transcript https://alt-5c5afaf83f339.blackboard.com/bbcswebdav/pid-2533770-dt-... Some people are so symptomatic that they're just not in a place where they can connect with and bond and bene!t from a therapist, so they need to start out with pharmacotherapy. But you always want to introduce the topic at the !rst visit, and then as they start pharmacotherapy and the mood starts to control a bit, then you keep discussing pharmacotherapy. And very often, once patients start to feel a little bit better on drug therapy, they're more open and receptive to a therapist and then can get to a therapist and interact with one. And depending on the nature of their disorder, sometimes-- [coughs] -- excuse me, the therapist can work with them in such a way that they develop the skills to manage their symptoms and can eventually be weaned o" of drug therapy. And other people's disease has a strong biologic component, and while therapy will improve their circumstances, they do have to stay on pharmacotherapy for the long haul. But the bottom line is best outcomes, really, is with both. And I think that's all I have for your key points. Now I would refer you to all of the wonderful learning exercises you have in the rest of the unit and, of course, the next video lecture. Print this page 18 of 18 11/2/24, 2:58 PM