All right, good morning, everyone. It is good to see so many people here in morning session, maybe not the earliest morning session on the last day of the conference, but still nonetheless a morning session on Wednesday of the conference, so something that we love to see. So my name is Colin Truitt. I am a member of the Scientific Programming Committee and a practicing psychiatrist in the D.C. area. It is my pleasure today to introduce one of our last clinical updates talks. Perhaps some of you have already been to the clinical updates series, but just as a brief reminder and plug to make sure that we do it again next year is we brought back the clinical updates series last year in New Orleans and it seemed to be a big hit. This is the meat and potatoes kind of section of education that we hope can give you updates and exposure to perhaps aspect of the psychiatric practice that you may not be encountering every day in your practice and enable you to feel more comfortable when you do come across these various faucets of the ever-increasing diversity of our field. A couple of quick reminders. We will be loading the slides into the app so you don't need to pull any paparazzi with the slides that you find interesting. We would appreciate minimal distractions there. We are aiming for about an hour talk and we'll be doing a question and answer session at the end. I'll remind everybody that because this is being live streamed that it's easiest for us to hear you and for people at home to hear you if you're using the mics for questions. So we'll ask that you line up there. I will also issue a reminder that we will be alternating between questions from the audience and also questions from our virtual audience up here. So with that, we may get a lot of questions. We try to ask that questions that are formulated be able to be responded to in one to two minutes by the presenter just so that we can try to get through as much information as possible. So with that and all of our housekeeping items out of the way, it is my pleasure to introduce our talk today of Chronic Pain for the General Psychiatrist, a Review of Shared Mechanisms and Treatment Strategies. And I am very fortunate to introduce Dr. Javier Jimenez. Dr. Javier Jimenez is a Director of Consultation Liaison Psychiatry and Chronic Pain Consultation at Long Island Jewish Medical Center. He completed psychiatry residency at the University of Pittsburgh Medical Center followed by a psychosomatic medicine fellowship at Massachusetts General Hospital, Harvard Medical School. Prior to joining Northwell Health two years ago, he worked at the Cleveland Clinic for seven years and was Medical Director for the Chronic Pain Rehabilitation Program. He is a board certified in pain medicine, addiction medicine and psychiatry and remaining academically active in each. And I have had the pleasure of hearing him speak when I was a resident at our EVA Grand Rounds. And so I think we are in for a treat today. So without further ado, I introduce Dr. Javier Jimenez. Thank you for the warm introduction. Good to see everyone. I'm humbled by the attendance. Don't take pictures of the slides, but if you wanna take pictures of me, that's okay. I have no disclosures to report financial or otherwise. I do wanna get into it because this is a big topic with probably something that we can talk about for hours and hours. So think of today as a little bit of a primer. I'm going to give a little bit of context as to how I became interested in this space and specialize in this space. As mentioned, my background is in CL psychiatry and I would throw myself masochistically at all sorts of complex problems, whether it was conversion disorder, factitious disorder, complex trauma, things like that, atypical medical presentations. And I was asked to take over a chronic pain rehabilitation program, an innovative program at the Cleveland Clinic that I'll speak about later, with very little or minimal pain management training. And I was pretty daunted at first, but then I realized that background in CL psychiatry and psychiatry in general is actually very relevant for chronic pain, which we'll get into. And in that space, I offered care in three different ways. And I invite people who are going to cultivate this as part of their practice to do the same if they can. One was in the CL inpatient setting, giving consults that were sort of pain psych, addiction blends, the kinds of consults that some other psychiatrist might shy away from and say, well, that's an addiction consult or that's a pain management consult, bridging these worlds, because you know, there's quite a bit of comorbidity between these areas, was needed. And so that was one thing that I would offer. The more important role that I had was medical director of the chronic pain rehabilitation program, which is essentially a day program with multidisciplinary components, physical therapy, psychological therapies, detox, pain psychopharmacology, which we'll go through, and other modalities. And then finally, I had also a clinic, of course, for individual cases who did not need a full day program of sorts. So think about that contextually as we go through the material today. And then you might ask yourself at times, why should a psychiatrist be involved with pain management at all? Firstly, I wanna make a big distinction here between acute pain and chronic pain. That's what really this is gonna be about, is chronic pain in all of its myriad forms, comorbidities, problems. When you think of chronic pain, then definitely there's a role for psychiatry in many cases, if not most. Secondly, we can recognize and manage psychomorbidities, obviously, better than an anesthesiologist, a neurologist, some of the other specialists who deal in pain management regularly. Thirdly, we are usually adept at psychopharmacology, and much of chronic pain management is applied psychopharmacology, which we'll get into. This is highly relevant, excuse me. So is detox, by the way, removing certain things that are contributing to disability or psychomorbidities, which we'll get into. And fourthly, we have some psychotherapeutic skills, compared to our other medical colleagues, and this is also highly relevant in this space, because there's gonna be quite a bit of transitioning of goals in chronic pain management, from what I call the sort of peripheral targets of analgesia to more central or integrative targets of functional restoration. That's a lot of words there, but that's what we're gonna unpack today. And somebody with a psychotherapeutic background, even if you're not an expert in psychotherapy, is already ahead of the game in working in this space than, say, a pain anesthesiologist or a neurologist, et cetera. I wanna remind everyone briefly of how prevalent depression and anxiety, not to mention other psychiatric disorders, are in certain pain syndromes. As you can see, I'm not gonna read every number up there, but you can roughly summarize this slide as saying that about 25%, at least, of patients with these various pain disorders will have depression and or anxiety. That's a huge number. Obviously, it can go even higher than that, sometimes 50, depending on what ailment we're talking about. Hooten is actually an interesting author. He's both a pain physician, but also a psychiatrist. He did both residencies over at Mayo Clinic, and he was the president of the American Academy of Pain Medicine just last year, which is an interesting kind of development, having a psychiatrist involved with that level of advocacy. His work, I strongly recommend looking into the epidemiology of chronic pain and psychiatric disorders. I flashed this slide to begin with this context that you are actually far more relevant than you might think. The question is, how do you bridge the gap and actually reach the patient who is very focused on pain matters? Before we do that, we should get some foundational definitions out of the way in terms of pain and what we're talking about so that we're all on the same page. The International Association for Study of Pain, which is the international expert at studying this and defining pain, has this definition recently updated in 2020, which I'll read verbatim, is that pain is an unpleasant sensory and emotional experience associated with or resembling that associated with actual or potential tissue damage. It's a little clunky, but what it means essentially is that first of all, there's a physical component. Second of all, there's an emotional component, not maybe there's an emotional component. There's always an emotional component. And it can be associated with real tissue damage or the threat of it. So you can already start to sense if your psychiatry brains are activated that there is an anticipatory effect here that could be very relevant as a clinical target for us. The function of pain obviously is evolutionarily adaptive to warn us from future harm. And if you will, we're gonna talk about this today, you want to examine the individual's subjective experience of pain and see how much of it is a combination of physical sensations, emotional reactions, not just to the pain, but to the event that led to the pain, whether it's an injury, an accident, surgery, et cetera. Please keep that in mind. Again, that experiential component is something that psychiatrists and other professionals, I'm sorry, I mean to include all mental health clinicians, might be more keen about or aware of, excuse me, than a neurologist or pain anesthesiologist. As a quick reminder of our general pain pathways, we're not gonna look at this too granularly, but I am gonna flash a few images just to get us all on the same page. Remember that pain is experienced as a peripheral phenomenon usually, and there are peripheral activities or actions going on in terms of nociception at the receptor, then transduction, transmission through the spinal cord, that's a cross-section of it, and then it goes up into the central nervous system structures of the brain. Remember this very simple schematic because you might be walking around day in, day out with this schematic in your head, but remember, patients are not. Patients are not thinking about the central structures involved in pain processing. Rarely are they. And one major intervention, believe it or not, as unscientific as this sounds, is educating them about this because once you open their eyes to the fact that there's more to pain processing than the knee, the back, the foot, then you can open yourself up to targets, which is where we get into our management strategies later. I wanna show another image that I like even more, which is focusing not so much on the periphery, but on the two central nervous system structures, spinal cord and brain, specifically the blue end over there, the descending pain pathway. We're gonna return to this time and time again in today's conversation because this is a clinical target for us to think about when we see a patient with chronic pain. It's something that we're gonna use our medications and different management strategies around. And it's also something to teach, once again, your patient about because this is an endogenous pain relieving or pain modulating arm that each of us has and everyone in this room, or hopefully most people in this room, have a pretty robust and strong one. But when you have somebody with chronic pain lasting years and decades and they're on controlled substances and they're deconditioned, they may not have a very strong descending pain pathway. And it's all about educating them about building that back up. Couple of definitions on pain classification. This is a little bit sort of tongue in cheek and funny, but the idea that most of us have a working model of nociceptive and neuropathic pain, and then there's all this other stuff, right? Especially overlapping stuff that can be very confusing and disorienting. Most physicians can cite the first two categories, but not a lot else. And so today we're gonna just briefly review these in a more organized way. I'm gonna offer the following that when somebody is presenting with pain that's in quotes the complaint, the first thing to ask is how long has this been going on? Let's think temporally, not the type of pain. Temporally first, is this acute or chronic pain? Acute pain being defined as under three months, sometimes under six months, depends on the definition you see from the initial injury or medical process. Whereas chronic pain is past three slash six months. Ask yourself if there's a component of central sensitization, which we'll get into later and unpack that. And then after that, ask yourself, okay, what are the pain subtypes here? Is it nociceptive? Is it neuropathic? Or is it so-called central pain? There are a few clinical examples listed there for each of them. We'll go over this, and I'm sure we can discuss this later in the Q&A, but I would strongly recommend thinking about it first temporally, then looking at what the type of pain is. And the reason is because chronic pain, as we'll see in a minute, needs to be contextualized, needs to be looked at in a very different way than acute pain, of course. In terms of definitions, as mentioned, acute pain is under three months or under six months at max. And it usually resolves with the expected healing process. Chronic pain, however, lasts longer than that. There is a definition of subacute pain, of course, between three and six months, but clinically, in my experience, it's not utilized as much or as helpful. And then I'm gonna share this very quickly as a tool, not so much for us as clinicians, but as an education tool for our patients, because education, as you'll see time and time again, is very critical in helping the patient understand why they need to address their psychiatric care. Teaching them about the different pain types, sometimes with a very simple and accessible analogy, can be very helpful. The analogy of a doorbell can be very helpful in this regard, where we think of nociceptive pain as something that's activating a peripheral receptor or the button of the doorbell, right? And that results in pain or the bell ringing, if you will. A neuropathic pain, however, is secondary to a lesion along the conduits, right, or along the pathways. And so that could be a problem with the wires that go between the button and the bell, if you will. And that can result in a variety of sensations beyond pain, right? Numbing, paresthesias. So the analogy here is that maybe you have weird sounds or muted sounds, things like that. And then finally, central pain involves the actual bell itself, if you will, or clinically, central nervous system structure, spinal cord and brain. And this is where you have massive reorganization of pain pathways and really abnormal phenotypes. So the doorbell analogy here would be that maybe the bell is just ringing on its own, right, with no peripheral activation. I use this to sort of solidify the difference between peripheral and central nervous system structures along the pathway, and patients can really relate to this and appreciate it. So I walk them through the image in the bottom, but also give them the image of a doorbell. I'm going to jump a little bit here to a topic that we might revisit later, and that's the idea of certain central sensitization syndromes. We're gonna define central sensitization in a second. I know it sounds like I'm going backwards, but central sensitization syndromes are a little different from the first three categories I just showed of nociceptive, neuropathic, and central pain disorders. Central sensitization syndromes are not even a fully accepted category quite yet, but we're starting to appreciate that these conditions that were formerly termed functional somatic syndromes, and even before that, somatoform syndromes, have enormous amounts of central sensitization as experimentally demonstrated. I'm not gonna get into that data right now, but each of the syndromes around this circle have shown elements of central sensitization with experimental processes, whether it's IBS, fibromyalgia, migraine, et cetera. Now, a room of psychiatrists should already recognize that these individuals, sadly, have enormous psychiatric comorbidities, and some of the theories, including the one that I'm sort of schematically flashing up here, suggest that maybe this is all part of one syndrome, and that we could be targeting these conditions jointly, not separately. We'll return to this later, but this is a separate category of pain syndrome beyond nociceptive, neuropathic, and central, and it's beyond acute and chronic. I would argue that most of these are chronic, almost by definition. It's very rare to see acute IBS, for example. That doesn't really exist. But point being, this is a separate category that we're gonna get into. So with all of this in mind, let's just remind ourselves of the context that we're in with the opioid crisis and the attention to non-opioid strategies. Remember that most of pain management, and this is not only for anesthesiologists, by the way, but any physicians, most of pain management is focused on analgesia, right? So a patient comes in and says, I'm hurting, I'm hurting. My pain is 10 out of 10, or nine out of 10. Our instinct, all of our instincts, is to try to alleviate the pain, and we should. We should continue to try to do that. That being said, it sort of hijacks our brain. It distracts us from the bigger picture and asking ourselves, what's driving the chronic pain? What are the underpinnings of this? What's the background noise, if you will? And so that demands, basically, a better understanding of what chronic pain is and what drives it. So let's get into that. So remember this definition from earlier? Same definition, right? I'm going to offer a little bit more that is offered by the same International Association of Study for the Study of Pain group. I'm not going to read everything on this slide, but as you can see, there are bullet points, six of them, about different individual features of pain, the fact that there are biological, psychological, and social variables, the fact that pain may not be easily expressed or clearly expressed by a patient. So it really complicates the matter. And what they're really getting at with these additional six points here is that chronic pain is complex and it's something that demands, again, additional input from different disciplines, a multidisciplinary sort of assessment. This is an invitation for us as mental health providers, psychiatrists, psychologists, others, to get involved and to try to assist with this Gordian Knot. So when we see chronic pain, my invitation to you is that we quickly try to contextualize things. And today's talk is going to give you some, hopefully some deliverables on how to contextualize rapidly, rather than just say, I need to find something that's gonna help with pain. Because then we're just gonna give some Balta to everyone, right? Let's be real. And we're gonna get to some Balta later. But we need to think broadly, more beyond that. That's not helping everyone. It's helping some people, but not everyone. So we need to think about biological processes that are at play, primarily central sensitization, which we'll unpack. We need to think of psychological dimensions, excuse me, that are at play, primarily anxiety in the form of what's called pain catastrophizing. So we'll get into that in a minute. I've selectively bolded three of these things, because there's so much, of course, that drives chronic pain. But I would attend to one of each of these, biologically, psychologically, and socially. Finally, the last one is the incentives, if you will, the behavioral incentives that are maintaining a chronic pain disability state or identity. This is very complex. We'll get into incentives in a minute. But the ones that I think that we can make the most impact on is, especially as solo psychiatrists, if we don't have much support, are items one and two, the central sensitization and anxiety items. So let's get into it. This schematic is a little busy, but it's a nice demonstration of the, mostly biological, but also psychological variables that perpetuate or maintain chronic pain, the risk for that, starting with genetic loading, so you're predisposing variables, then perpetuating environmental stressors, traumas, then psychological strategies or traits or tendencies, like neuroticism, poor impulse control, catastrophizing, these kinds of things. This should look pretty familiar to you, because it's also relevant in other psychiatric disorders. Same thing with chronic pain. Not everyone who develops an injury is going to develop chronic pain, so you have to ask yourself, what is it about this person's diathesis, or risk profile, that has led to this perfect storm? I mentioned already, once or twice, this term, central sensitization. I'm finally going to define it formally. You may already be familiar with this term, but it's gained a lot of traction in the last 20 years or so. It's basically the phenomenon of abnormal, enhanced pain signaling in the nervous system, particularly in central nervous system structures, like the spinal cord and the brain. And this phenotypically presents itself with two presentations, if you will, or both. Hyperalgesia and aledinia. And these are important for you to know as a psychiatrist, because if you use the terms hyperalgesia and aledinia, you're going to already be speaking the language of pain. And that's very important when your patient is coming with that agenda in mind. Hyperalgesia, as the name implies, means that you're feeling more pain than is expected for a given stimulus. This is classic in fibromyalgia, where somebody may be fatigued, or they may bump themselves, and now they have lingering pain beyond what you would expect. And it's classic, for example, an applied form of hyperalgesia is photosensitivity in migraines. Normal amounts of light are causing pain. So you see hyperalgesia actually in many, many examples, but we rarely think about it as psychiatrists. Aledinia is a little less common. This is where one experiences pain when they shouldn't feel pain, based on the stimulus that is activating that individual. So that could be clothes, or the wind, or water. Something very subtle could be activating pain. Usually in the second category of aledinia, there's been some reorganization of pain pathways, and it's a more worrisome and more difficult thing to treat. From a neurobiological standpoint, there is this phenomenon of wind-up or temporal summation involving NMDA receptors that I'm not going to get into. But this has been experimentally demonstrated. It's a very real thing that happens over time. It does not happen overnight. But central sensitization is argued to be implicated in many of these syndromes, particularly chronic ones. And that's what we're talking about. And those who are very disabled from their pain, you can essentially assume that they have an enormous amount of central sensitization, which is important as you try to reach them and try to help them with their pain. These are schematics to remind us of normal pain action potentials when a noxious stimulus activates the nerve and you feel pain at the end there, or when you feel touch with a light stimulus, something that should not activate pain. However, in central sensitization, you have abnormalities here where the same stimulus activates a stronger action potential. And with allodynia, you have a reorganization as you see the arrow going back up towards the pain neuron. So now you have abnormal reorganization there. This is one of my busier slides, but I think it's a really integrative one that shows how central sensitization could be interacting with a bona fide organic ailment. In this case, we have an example on the bottom left of rheumatoid arthritis, of a neuroinflammatory environment with cytokine storms, very real nociceptive activation in the periphery. However, that is also causing neuropathic injury because it's very close to the receptors or the rest of the conduit. And so you have both nociceptive and neuropathic kind of components to this pain experience. To further complicate things as you go further up in the diagram, you see the spinal cord and brain. These are your central nervous system pathways with hyperalgesia and aledinia informed by various changes over time. I'm not going to read every word, but it very beautifully captures that. And then finally, the top box is your sort of forebrain or cognitive contributions to a pain experience, which we're going to get into in a second because it's highly relevant for the psychiatrist. I show this not so much for education for patients. This is a little convoluted for them, but it's helpful for us to integrate this dynamic interplay. I'm going to flash a couple more images and then get into the meat of pain experience, then transition into pain management, some strategies that we should think about with our patient, and then eventually segue into Q&A. So this image is just a reminder that even more complex than I earlier showed, the up-down sort of regulation of pain involves numerous pathways. And as you can see, it involves limbic structures, not just your sensory relay station in your thalamus and your descending pain pathway, but there's actual forebrain contributors to pain processing. This one's even glossier in that it shows the various brain structures that are involved with pain processing. That's in red, strictly pain processing. And then those that are both pain and mood, that's that orange mustardy color. And you can see the sort of blurb on the right basically summarizes that studies have shown time and time again that areas of the limbic brain, including the anterior cingulate cortex and other areas, are implicated in both of these processing phenomena, insular cortex, et cetera. This is a so-called neuro matrix of pain. If you want to learn more about that, it can hurt, of course. But I think at this level, it starts to get a little bit beyond what the patient can kind of access and understand. It's just important for us to know as clinicians that there is abundant evidence to show that these areas are implicated with pain and psychiatric disorders. So this gets us to the idea of a sensitized brain, right? And this is something that we deal with all the time in psychiatry. Brains that unfortunately, for various reasons, have altered neural pathways, have been sensitized, genetically loaded, et cetera. The same thing can be said of those with chronic pain. They may have a diathesis that they're walking around with. Then they have an environmental insult. And then it opens the sort of floodgates for a sensitized brain model. And I would invite that everyone start to think a little bit more about PTSD, frankly, as a model to better understand your chronic pain patient who is circling the drain and is very hypervigilant about their pain. They're avoiding different activities or different things that could activate the pain. And they have increased hyperarousal, right? The three cardinal features of PTSD. You see this time and time again in your very disabled chronic pain patient. And it's a very useful model to understand if there has been a sort of top-down dysregulation from cortex to subcortex. And I see it clinically all the time. Furthermore, this has also been vetted with fMRI studies that show that PTSD patients and those with chronic pain without PTSD have shared neural pathways. So I'm not going to unpack all of that research data today. But if we take that at face value, then we understand that many of our chronic pain patients may be behaving very much like a PTSD patient. However, they may not be consciously or overtly aware of perpetrators or violence or motor vehicle accidents or other things like that that we routinely hear in PTSD. Here, the trauma may be the pain itself. This schematic is meant to remind us of that, that really anything that is presented as dangerous could activate our fear processing pathways, including our amygdala, through the shortcuts that are subcortical without much cortical input if we don't have that top-down regulation. Now, imagine if pain itself is the thing that is scaring the individual, that is threatening them. And remember the International Association for the Study of Pain definition that pain can be defined as not only something associated with a lesion, but the anticipation of a lesion. Remember, somebody's experience of the initial pain can be so traumatizing that now any experience of a pain symptom, rebounding, or we'll get to this later, even withdrawal, we'll get to opioids later, any of these little things can activate them so strongly that it can really dominate their behaviors and their choices thereafter. So you have this summative pain experience informed by this kind of PTSD model. Does every person with chronic disabling pain have this phenomenon at play? No, but I contend that if you do this long enough and see enough patients, you will see this time and time again. Some form of an altered pain experience involving fear, anxiety, pain catastrophizing, which we'll get to. So it's important to have a very cursory working model around pain experience, and the first step for that is to understand a little bit of pain psychology. This is just a few slides dedicated to this. There's a whole field of pain psychology and psychologists that dedicate themselves to this and research it, et cetera. But I'm going to offer a quick mnemonic in a minute as to how to think about that when you're in your rapid assessment of patients. So remember that pain can be experienced viscerally as a threat, and it can inform how somebody recovers or doesn't. The schematic on the right shows a binary kind of path of recovery from initiation of pain based on pain experience. That's the fork in the road. If somebody has a quote-unquote normal or usual or less than valenced pain experience, then they're going to confront recovery and do PT and wear the cast and do all the things they gotta do and hopefully bounce back. And that, thankfully, is a majority of people. Most of us, thankfully, are armed with the resiliency to bounce back from these injuries or surgeries or whatnot. However, you have the other path when somebody has a very valenced, negatively valenced pain experience that can lead to things like pain catastrophizing, depression, now avoidance, misuse, deconditioning that's physical, fear of movement, agoraphobia, all these various phenotypes, and avoidance through not just lack of activity but controlled substances, right? Opioids, benzos, et cetera, which we'll get to. And so think about that pain experience. See if there's anything that we can do about that cycle to break that and get them back into a recovery path. This is actually what we did time and time again in our Chronic Pain Rehabilitation Program with the large team that we had to sort of get them back into a more normative or adaptive pain experience pathway. So this slide is just a reminder to think about somebody's pain experience and ask yourself how much of this pain experience is predominantly neurological, physiological because of their pain syndrome, whatever you might know about it, records you reviewed, their exam, et cetera, and how much of it is psychobehavioral. Remember that it's always a little bit of both. It's always a little bit of both or a lot of one and a little bit of the other, but it's never a true binary, in my experience at least. And one quote that I wanna leave you with here that's very important is something that we would use all the time in our, again, clinical setting is that chronic pain is a very real medical and neurological phenomenon because, again, central sensitization and all these processes are underway. You do not wanna communicate that it is not real or that it is psychogenic, any of that. However, pain disability is heavily informed by psychobehavioral changes, right? And this is the pain psychology we're gonna get into. It does not mean that this is a choice necessarily, but something has happened to this individual that does not happen to everyone that has led them to fall into this disabled state. So pain psychology. This is my mnemonic that I offer to trainees and to other clinicians who wanna learn how to quickly assess pain experience in their individual patient. It's the ABCs, which involves affect behavior, cognitions, and social environment. And basically the corresponding pain psychology research vetted analogs to this include pain distress, that's the language we use in pain psychology, pain avoidance, which we'll get to, pain catastrophizing, and then finally, under the social category, it's pretty messy, but the language of enabling incentives, things like that. So each of these is listed here very quickly. I think each of you can deduce what these things are, but I do wanna highlight a couple of details. With affect, it really is mood, anxiety, in a bread and butter kind of way, and I think psychiatrists are well prepared to sniff that out. With behavior, however, again, I think we should be attending more to avoidance patterns, right? That could be fear of moving, fear of engaging with the world, but also fear of feeling things, and that means the individual dousing themselves, self-medicating, if you will, or using other medications that are very suppressing, CNS suppressing. Cognitions, the catastrophizing construct is very important. Catastrophizing is something that we all are familiar with through CBT and other thinking distortions, but it's really prevalent in chronic pain and has been shown as one of the poorest prognostic factors for a patient to do well. This is where it could manifest as somebody thinking that their body is falling apart, they're gonna die, things of that sort, I'm always gonna be disabled. If you sniff that out, then it's a very important target, and if you don't address it or try to, that person's gonna continue to languish. So a couple of things that I'm gonna just very quickly mention. This is just a PHQ-9 and a GAD-7. I'm not gonna review this. There are more pain-specific type screeners out there, but I think in this audience of psychiatrists, it's probably fine to use any of the vetted depression and anxiety screeners for what we call affect, the first letter of the mnemonic. However, for behavior, I do suggest getting familiar with something called the Pain Disability Index. This is a well-validated instrument that is publicly available that looks at pain behaviors across seven dimensions and assesses whether somebody is totally disabled by that, partially disabled, or not at all. Very important conversation starter when you're seeing somebody, if you wanna integrate this into your clinic or whatever practice, because you might see that somebody is, for example, 10 out of 10 occupationally impaired, but they're not impaired at all in the other domains. So that's a bit of a red flag for malingering, if you will. Whereas if you see somebody who's only sexually impaired, but everything else is fine, that may connote some complex, interesting relational issues. So there's a lot of interesting data that can be collected from this, and it might even build some insight in your patient if they fill this out. The pain catastrophizing scale is the next one that does capture these distortions that I mentioned earlier. Again, if somebody scores high on this, you're looking at a poor prognosis, and you need to do something about that quickly. Then finally for S, the social category. There's no real great scale for this. I invite everyone to be curious about environmental factors that could be enabling, facilitating, reinforcing disability. There are time and time again all sorts of dynamics out there where individuals might have a chronic ailment, not just pain, any disease, and the family members might be contributing to disability, sheltering them from doing activities, things of that sort. That usually doesn't help, unfortunately, even if it comes out of a place of love. So think about that much like you would with, for example, addiction work and looking at enabling. Also look at incentives like disability applications, lawsuits, workman's comp. There's a rich body of evidence that individuals who are in the midst of a lawsuit or application for disability or workman's comp case tend to do poorly with pain interventions because either consciously or less than consciously, they have something to gain, of course, from not doing well in terms of remuneration and rewards. So I just invite here, of course, to be clinically curious, be a little bit skeptical of what they present, but also compassionate and review records, get collateral if you need to, get more objective stances on somebody's functioning. There is one scale that I think can also be useful which transitions us to our management in a minute, and that's the ACEs scale. I think that it can really open up the conversation for patients to realize that maybe some of the things they knew happened a long time ago might actually be connected to what's happening now. Trauma, adversity as a child or as a young adult could be catching up with them. And so it also captures, of course, all forms of neglect, and I'm sure you're aware of this scale. It can be a good conversation starter and lead to conversations about neural priming, central sensitization, and then why you, as the new physician that this person is seeing, is interested in managing these other areas. I'm not gonna spend a lot of time on this, but there's a rich body of evidence on using CBT for certain pain situations, chronic pain, things like that. There's also a bit out there on psychodynamics. Be curious about these entanglements, enactments, between patients and their families and their providers, because it could be informative as to why they're sort of circling the drain, utilizing care excessively, why they might be so affectively charged, maybe angry, things like that. So I won't get into this too much. Trauma is quite central to helping or identifying and unlocking the trauma is quite central to helping the individuals with these kinds of presentations. So I know I glossed over pain psychology very rapidly, but I just wanna leave some time for Q&A later. If there are questions about that, conceptualizing the individual rapidly, either through instruments or other mnemonics, please bring it to the Q&A part. So now let's talk about management. The first part of the talk has been a lot about understanding what is chronic pain? What are we looking at? What is this individual's pain experience? What is this individual's pain psychology? Now, in our heads rapidly, in the same session, we need to somehow translate all of this back to the patient and reach them. And that's what I mean by bridging the gap. Because if we just come at them and say, you know, your trauma and your stress is catching up with you, you're gonna lose them, right? They're all about pain, pain, pain. So we need to come across as practical and reach them. So remember that the patient's perception and agenda is my body hurts, my leg, my foot, whatever, my belly, and treat it, do something about it, doc, or can you do anything about it? You're just a psychiatrist, right? That kind of thing. And this is a peripheralist sort of perspective. My advice is that you immediately, very rapidly, and confidently, when you feel confident to do this, say, I can do something about this, and here's why. And then the first step is to educate them about pain pathways in a very jargonized, very medically accurate, but jargonized kind of way. And now this is a little bit of the sort of smoke and mirrors performative part of this, right? You need to be the person that really convinces them that you have something to offer. And it involves, very initially, with this neurovalidation or medical validation process, understanding pain pathways, understanding pain syndromes, which we're not even gonna define all of the different categories today. Doing all of that, I think, is critical so that you do not lose them. And like that, you don't start off with trauma and stress and that kind of stuff. And educating them, literally, with an image, if you have one in your office, keep it handy. I have images like this in my office so that the patient understands that pain processing is rather complex. And there's more targets here that the orthopod and the rheumatologist and the neurologist are not gonna address. You might be able to, right, as a psychiatrist. So now you're opening them up to options. And that's the first sort of initial step to get into psychopharmacology, which we'll get into. A reminder of these two images. The reason that they're side by side is because the one on the left is a great starting point for patients who have no concept of pain pathways. But I think you also have to jump to the one on the right. Remember, the one on the right is more of a centralist perspective. It's the one that reminds them that there's a descending pain pathway with endogenous opioids, things like that. You can use language like, you know, you're endorphins, you've heard about these. When you do exercise, you feel good. Use that kind of lingo to reach the patient and they start to understand that there's something neurobiological that you want to manipulate with your treatments to help them with their pain. And that can be more effective usually than saying, I'm gonna try to help you with your depression. Because if you might have already experienced this, most people say, yeah, I'm depressed because I'm in pain. And so let's get past that and try to really actually help them with the neurological underpinnings of their pain through management of that central sensitization. As far as treatment for chronic pain, there are some chronic pain syndromes, although they're rare, that can be quote unquote cured. However, when you're seeing somebody with years duration of chronic pain that is complicated by comorbidities, disability, polypharmacy, the emphasis should not be on cure. It should be on management and on what's called functional restoration or rehabilitation. This is where we meet a patient whose life has been robbed by the chronic pain or the treatments of the pain and you invite them sort of existentially to get their life back, right? And so that's the goal is to rehabilitate them, get quality of life, get moving, get active, that kind of thing. Get free of some of the things that are limiting them. The target here then is rehabilitation and I categorize rehabilitation into three categories as medical physicians will probably get more involved with two of these, the medical and psychological rehabilitations. However, we might refer or recommend physical rehabilitation and I don't just mean PT in a conventional way, but we might recommend that because we might understand that this person needs to get behaviorally activated and moving. So I have a lot of jargon in there for each of these categories as to things that the patient may need. Now each patient needs more or less of each of these categories, right? Not all of them need every single thing that's listed there. You're gonna have to address that based on what you're observing. But I suggest bringing up these three aspects of rehabilitation or management for your patient because rarely with somebody who's really disabled, moderate to severe, well, they do fine with only one of them. And I think the temptation for all of us is like, well, let's just manipulate the meds a little bit. We really need to give due credit to the other two. So with that being said, I am gonna focus today for the rest of the talk and then we can have Q&A around this as well around medications. It turns out that a lot of the medications we use in psychiatry have a role in different chronic pain scenarios. And not just the medications we use, but also our training and understanding how controlled substances should work, should not work, their adverse effects, et cetera. Pharmacologic creativity is the norm here, not the exception. Meaning there are not many FDA approved antidotes for complex chronic pain, right? So here we're gonna have to be looking at, again, comorbidities and different things like that and using the medications intelligently, a little bit of trial and error, unfortunately. Where I come from in CNL, this is standard, right? We're managing conditions on the medical side. We don't have FDA approved treatments for agitation, delirium, things like that. So we're kind of used to that. The other thing to consider is removing barriers first. Now this is complex. You may have some luck doing this if a patient trusts you. But opioids, benzos, marijuana, some other substances may be in the way in this population. And people might be really wedded to them for reasons that predate your visit. However, we're going to talk briefly today about why we should consider removing these. They're a big obstacle for any of our other meds to work and frankly for the patient to get better. Then we're going to go over the various classes of meds that you might anticipate have a role in pain management. Antidepressants, I think, are very familiar to us as are anticonvulsants, antipsychotics less so, sympathetic modulators as I call them. It's kind of a silly name for alpha and beta active medications. And then of course, suboxone or buprenorphine naloxone may or may not have a role in analgesia. We'll go over that. And finally, ketamine has been very popular as of late. So on this topic first of removing barriers, so obviously let's avoid chronic opioid therapy as much as possible. There's no evidence base for using chronic opioids in chronic pain. That was codified, explained, reiterated in the CDC guidelines in 2016. However, you may see somebody who's already on opioids. So the question is, how do we help them consider from a pre-contemplative to contemplative kind of journey, consider whether these meds are really serving them any good? And the conventional concerns that people usually reflexively say about opioids is that they're dangerous and that they have addictive potential. And those are very true. However, it is rare for a patient who has been taking chronic opioids to actually be concerned about that, in my experience. They are warped, unfortunately, by the opioids and think that they are exceptional and that they're not going to succumb to overdoses and things like that in addiction. That being said, a few other concerns may ring true to them or may resonate. And those are bodily harm, those are long-lasting effects like cognitive ones, changes in their immune system, things of that sort. And then the most important one in my clinical experience is the fact that opioids actually cause opioid-induced hyperalgesia. Remember that term? So if you actually can explain to a patient, and they may not have heard this before, that opioids cause, over time, up-regulation of receptors and you need more and more of it, and they actually cause pain, suddenly, if they actually receive that message, they may see that opioid as the enemy, right? And they might say, how do we make some adjustments with that? And there's evidence, by the way, scientific evidence to support opioid-induced hyperalgesia in both animals and humans. So we're not, you know, blowing smoke up their whatevers. This is real, and we should use that to hijack their agenda of pain relief, if you will. That's my suggestion, if you can. So the method is a complex blend of motivational interviewing, which I strongly suggest getting adept in if you want to do anything with chronic pain patients, some clinical confidence, being, you know, again, familiar and comfortable with the language, the jargon, and then, of course, a little bit of time. This does not happen in three minutes. So if you have a practice that does not allow for this, maybe don't take this on. But if you have the ability to spend 10 minutes, even, on this topic, you may be able to make a difference or move the needle a little bit. And as with all MI work, it's all about nudging them to the next level. It may not be a full home run all the way to action, but if we can move them along the spectrum, then maybe we've made some progress. Same thing with benzos. I just want to share a little bit of data on benzos because we know a lot about opioids and the harms recently associated with opioids. And as psychiatrists, we may know more about benzos than other disciplines, but it's really fascinating to see the epidemiologic studies that show that benzos actually predict worse pain outcomes than, you know, pain scorers or opioids or anything else. Really fascinating. So this is a real problem. The benzos, chronic benzos in this population do not solely focus on opioids. And the reverse is also true, that those who have high chronic pain scores are going to end up more often on benzos, put aside opioids for a second, to sort of relieve whatever they're going through. This is, again, another indication that perhaps their psychic experience of pain is laden with PTSD kind of components or anxiety or something like that. So I won't harp on that kind of data too long. I do want to sensitize people to another phenomenon known as Holy Trinity, polypharmacy, which involves a third category, not just benzos and opioids, but skeletal muscle relaxants. You might be doing your part, actually, in saving a life if all you do is have somebody get off of one of three of these agents. This is a poster that I don't expect you to be able to read that I presented at a pain conference of a young woman who was on carisoprodol, muscle relaxant, also known as Soma, benzos, and I believe methadone, and had a life-endangering, plural, effusion, and almost died. Had a chest tube drainage, all these dramatic clinical outcomes, and survived, and it turned out to be directly related to this polypharmacy and the respiratory suppressive elements. And so anyway, it's also known as the Holy Trinity, and the GABA synergy between the skeletal muscle relaxants and benzos in particular is pretty potent. Please be aware of this as a clinical entity. When it comes to weaning people off of opioids, let's just say that you actually have a patient, and it does happen. You might be thinking, this never happens, but it does happen, who wants to come off of benzos and or opioids, or narcotics if we want to call them that, you know, jointly. Then the issue that you need to do is sort of set the stage, right, with clinical confidence and competence, have that trust built very rapidly with the patient, reassure them that you'll be there for them, and then do some symptomatic sort of treatment, maybe preload them with medications that might help with the weaning process, and then go through the wean. This image is actually borrowed from a GI article on Narcotic Bowel Syndrome, which is a fancy word for narcotic addiction in GI patients, and some of the things that they would suggest doing. Of course, we are the psychiatrists, so we may not refer, but the point is that you might consider different interventions as somebody gets on less and less of the controlled substances, right? And there's a spiral in the end over there to remind us of the stages of change with MI so that we can try to shepherd the patient through these steps. The topic of cannabis and CBD, and I'm in San Fran, it's a boot. I'm not a fan. I just have not seen outcomes. And I just want to share a little bit of Cochrane Review-based information on this. CBD formulations have not met the sort of muster of the hype that we all wanted or still want around CBD for chronic pain. There's actually some evidence to suggest CBD can help with sleep and some other things. With pain itself, there's really not a lot of good evidence. There's poor methodologies. They actually exclude people who have psychiatric and or substance use problems, which is an issue for this audience, right? And so I think, you know, suffice it to say, we can debate this more later. There's very little hard, good longitudinal evidence that cannabis, especially unregulated cannabis or CBD is going to be a game changer in pain management, particularly in complex patients. There is some evidence, however, to show from a harm reduction standpoint, that it's obviously preferable to be on cannabis, marijuana, CBD than it is to be on opioids. And some people have used it as a stepping stone off of opioids. Obviously, in that scenario, you know, that's a lesser poison, if you will, a lesser harm. Maybe that's a transition, you know, that is that is beneficial. And remember also that cannabis slash marijuana is not the same as CBD, not the same as THC. There's a lot of messy noise out there, highly variable situations. I have a very wordy, opinionated soapbox editorial that I put out that I'm not going to read. But in here, I write from the standpoint of a psychiatrist about the issues with particularly unregulated cannabis and marijuana in chronic pain. That, number one, hasn't been studied well in our populations, our psychiatric populations. Number two, our folks have higher risk factors for transitioning into really problematic mental health outcomes. Number three, cannabis typically will rob individuals of motivation and energy, whether that's cognitive, behavioral, both, to do the things that they need to do to recover. So there's a variety of problems that I list here. I'm not going to go into all of it now. We can debate it later. But I just haven't seen it helping a lot of people in my clinic or in my experience. So let's get to pain psych, psychopharmacology. The Venn diagram here is neat, useful, attractive in that it lists all of our med classes, or most of them, into different buckets and sort of organizes what you should do if you see somebody with chronic pain. Now, of course, the temptation is to focus on the middle there and just pick a TCA or an SNRI, right? And they are valuable. We're going to get into that. But I would contend that essentially everything in this image, with the exception of maybe the benzos, has a role in chronic pain. We're going to get into that in a minute as to how and why. So it's all about using a nuanced approach. Let's go over the antidepressants. I'm not going to read this whole list, but these are a variety of conditions that have shown some at least modest evidence of effect for the use of antidepressants in treating pain. As you can see, there's a variety of conditions, and this includes all antidepressant classes, by the way, not just TCAs or SNRIs. I want to remind the audience that the reason that TCAs and SNRIs work and SSRIs don't, predominantly in pain management, is because of certain pain pathways in the descending pain pathway, remember that, involving norepinephrine and serotonin. You need sort of both neurotransmitters to be involved or implicated. And this has been demonstrated or reversed with animal studies. And so it's an important reminder as to why we're using this. If you have a sophisticated enough patient, you might even explain this to them and say, look, these neurotransmitters that are part of these meds are really essential for helping you with your pain malady, if you will. SSRIs thus are mostly ineffective in pain management. I put mostly because, remember, there's a lot of comorbidities that we're still working with here, right? Anticipation of pain, fear, all that kind of stuff. So we'll get to SSRIs a little bit later. I published a clinically anchored kind of narrative review on the use of tricyclics outside of depression for sleep, for pain, for GI disturbances, et cetera. I can't go over all of it today, but I welcome you to look it up. It has a review of our TCAs, how they're organized, tertiary versus secondary means, their side effects, their various pros and cons, their dosing ranges, and then more importantly, clinically, what you might consider in these various conditions and things to look out for. I think everyone in this room is roughly familiar with the first three columns, but the two columns on the right are the ones that we kind of sometimes limit ourselves with and say, well, all the side effects are pesky and they can be. But I would say that there are things that we can do to mitigate them. There are things that we can talk to our patients about to try to get past dry mouth or whatnot. And of course, it would be remiss for me if I didn't say that we should be careful with our impulsive suicidal patients because you don't want them overdosing on this, of course. I think a lot of psychiatric practice has unfortunately fallen back on the safety of SSRIs and SNRIs without broader use of TCAs because they are actually more effective in pain, believe it or not, than the SNRIs. Which gets us to the SNRIs. I am an advocate for using them in mild to moderate cases. However, they haven't been as effective, again, as TCAs. They are safer. They have less side effects. So there's that. But when you have a complex chronic pain patient who's really languishing, you might ask yourself, what's the tradeoff that we're all willing to live with here? This is also a Cochran review that I'm not going to read, but essentially suggests that in conditions like fibromyalgia and a few other pain disorders, the SNRIs were only slightly better than placebo. Not really terribly helpful. However, again, if you have a mild to moderate case and they've tried duloxetine effects or something like that and they're benefiting from it, then go full steam. But I'm talking about the more moderate to severe cases, which may not respond to that. Here are a few of our SNRIs listed. Again, this is just a summary statement because I have a sense, correct me if I'm wrong in the Q&A, that most people here are familiar with these agents because they're quite popular. So I don't want to spend too much time on the SNRIs and instead focus on some other alternatives. There's my Cymbalta kind of second soapbox moment. Cannabis and Cymbalta. Cymbalta is sort of widely prescribed and it's usually very safe and with good intentions. My whole problem with Cymbalta is that I've seen time and time again individuals who have longstanding psychiatric disorders, fairly controlled or even well controlled on an SSRI or some other agent, switched over to Cymbalta because a rheumatologist, a primary care doctor, someone out there says, hey, I can kill two birds with one stone now that you have pain. And then unfortunately, the earlier psychiatric disorder suffers and then the whole pain disorder suffers because now their anxiety or depression is worsened. So think about that, particularly in your, again, moderate to severe cases. I would say that we should be looking at the psychiatric priority here. So in an interesting twist, because chronic pain is so laden with depression and anxiety, SSRIs do have a role. And so you should consider that in terms of sort of indirect pain management. So this is just my statement on SSRIs. Remember the PTSD model, it's quite prevalent in our patients. If they have all that hyper arousal and hyper vigilance, maybe we can douse it a little bit with safely but aggressively dosing an SSRI. In my experience, most of these patients with chronic pain are highly, highly anxious. And so I try not to be ginger with the dosing. I try to be a little bit faster and get to that sort of nervous system that's on fire, if you will. So that's all I'll say on SSRIs. I do want to mention something interesting about bupropion. You wouldn't think that it has much of a role, and it doesn't have a large role in chronic pain, but there actually is a little bit of noise out there that it can be helpful in some neuropathic pain syndromes. Obviously helpful for things like fatigue, since it's so activating. And it can help in other depression states, obviously, with your comorbid pain disorders. So I just want to mention that to not forget it. Moving on to the anticonvulsants. So we use these a lot as mood stabilizers or other agents in psychiatry. As you can see, there's quite a bit of conditions, neuropathic conditions, etc., that respond in some way or to some degree to anticonvulsants. The mechanism of action, just to review, is varied in terms of different electrolyte channel blockade, not just sodium, but also calcium, GABAergic effects, and then mixed effects. It's just a fun, neat reminder of the action of each of those. I'm going to go over this a little quickly, just so that we can get to sort of, you know, Q&A after some summative statements. Some of these are going to be extremely familiar to you and even problematic in some ways, like GABApentin, for example, which is also very widely distributed. I think we're all familiar with Neurontin. Its evidence base is in those following conditions. And, of course, in terms of dosing, I would suspect that we're all somewhat familiar with it, twice a day versus three times a day, up to 3,600 milligrams a day. After that, it's essentially renally cleared and ineffective. Of course, use your judgment. In our psychiatric population, some people may be using this as a way to check out. It can be a blunt sedative. And you want to be looking out for things like encephalopathy, sedation, etc. Its cousin, pregabalin, is also an option in neuropathic pain syndromes, can also be quite anxiolytic. In Europe, the equivalent, the analog of the FDA in Europe has approved Lyrica or pregabalin for anxiety disorders, I believe generalized anxiety disorders. So there's something to that. And clinically, I'm sure you've seen some patients have reduced anxiety with pregabalin. So if they're responsible and can take it safely, why not? So there's some dosing information there. And where it's been found to be helpful, I'm not going to read every line. You got to watch out for things like delirium, rare withdrawal states. It's also something that is, you know, renally cleared. So be careful with those who have renal risk factors. A couple of other ones, topiramate also has some mood stabilizing properties, but it's actually quite helpful in headache management, migraine prophylaxis. If you go to a neurologic clinic or a migraine clinic, they use it avidly. You know, and so that's a usual use of it. But I've seen it also being used in other neuropathic states. And the problems with this, or benefits, depending how you look at weight loss, include weight loss, but also renal costification, stones, cognitive slowing. You know, it's affectionately known as Dopamax, etc. So you need to be careful of that. Carbamazepine, an oldie but a goodie, in my psychiatric experiences, I find it to be a very good mood stabilizer, can also be effective in neuropathic states. You see some of the conditions, but it does have its problems, right? It has a few side effects, and it can be, oops, skipped there. I don't know what, my slide is a little cut off here, I'm sorry. But there was mention there of what to monitor, and things of that sort, so. Oxcarbamazepine, its cousin, a little less complex. It does have less of a pain relieving property. You see less of it used in trigeminal neurologies and things of the sort, carbamazepine more so. But it does have a place if you've got a facial pain patient, for example, and they've not responded to other things, doesn't hurt to try. Lamotrigine, fairly common mood stabilizer that we use in psychiatry. Also, believe it or not, has a role in pain management in select conditions. Oddly enough, in post-stroke central pain, it's been shown to have a signal. I wouldn't say that it's gonna help everyone with post-stroke central pain. That's a very stubborn condition with very few options. But it has, according to a few open-label trials, helped. And so it's something to consider. Of course, you need to start low and go slow due to Steven Johnson's rash, etc. And be careful, see if it's also going to help with mood stabilization. But it's another option. Some of these meds are things that you're very familiar with, but you might not have known that they could have had an application in pain management. Cepakote or valproic acid is one of my favorites. Actually very helpful also in headache management, migraine prophylaxis, but also acute abortion of migraines and infusion forms, IV forms. It can be helpful in some stubborn neuropathies. Obviously, you need to look out for thrombocytopenia, liver injury, etc. I think we all know valproic acid fairly well. Interestingly, lithium actually has a history of helping with a subtype of headaches, cluster headaches. And so if you have somebody on that, happens to have that type of headache, which is not the most common, migraine is by far the most common, it may be doing two things for them. Also, as you know, has a strong anti-suicidal effect. Something that I didn't mention is that suicide rates, either ideation or acts, are much higher in chronic pain patients than in the general population. So it could be that you're helping them with some of the inevitable distress that comes with chronic pain and suicide if you were to somehow add or augment with lithium. Now I wanna talk about antipsychotics because they're not usually thought of as pain management options. This is where I did some research in their utility. Clinically also, I used them as adjuncts routinely in the chronic pain rehab program where I saw people with complex traumas, with all sorts of comorbidities. In low doses, they seem to help a lot. Whether that's ego glue, the old sort of terminology, or something else is unclear. But because of that, I then did a systematic review to look at the evidence behind antipsychotics. But before we get to atypicals, the newer ones, remember that Haldol has actually been used traditionally for acute pain states in ER settings, IV Haldol, for example, to abort headaches and things like that. When I was at MGH, I was on a burn unit, and I remember that we would couple dilaudid with Haldol, and it was more effective for dressing changes and the pain around dressing changes than just dilaudid. So maybe it's just addressing the psychological dimensions to that, the fear. But nonetheless, it could be your friend in certain clinical states. I don't know much about PO-HALD, although, in terms of pain management. And then in terms of atypicals, remember they have a heterogeneous receptor profile, right, more so than the typicals, in terms of touching up on these other areas. Maybe that has something to do with helping with pain, just like the TCAs do, right. They're very messy from a receptor standpoint. The dosing I would recommend is much lower than you might use for bipolar disorder, schizophrenia, things like that. Unless, of course, the person has that condition. But if they don't, and you're trying to augment an existing TCA, something else, then you might really start low and slow. And this is not your first option, as I'll show an algorithm in a second. This is a review that I mentioned. We basically looked at, systematically, at all trials, case reports, retrospectives. There's not that much out there, but what was out there about antipsychotics, particularly atypicals, applied to pain settings or pain symptoms. And the studies that you see on the left there are those involving olanzapine or Zyprexa. And it was the one with the most studies. Usually, research sort of follows some kind of clinical observation. They found that with olanzapine, there was modest to good signal of efficacy in certain states, fibromyalgia, migraines, central sensitization syndromes. Again, an augment sort of formulation. These are the other studies. There were far less of them, quetiapine, aripiprazole, risperidone, etc. Not a lot can be said about these other agents. There is some budding evidence that maybe Seroquel or quetiapine can have a role. But as you know, that medication covers so many bases and is bluntly sedating and anxiolytic, so maybe it's doing something different. So in that article, I share, you know, the usual reminder, because it may not be psychiatrists who are doing this, right? It may be other doctors who might give low-dose antipsychotics the usual reminders of what to monitor over time with the use of antipsychotics, weight, metabolic profile, EKG, etc. Obviously, if you have somebody already on a TCA and you're adding an antipsychotic, you've got to be extra careful in terms of QTC, weight, etc. This is also an algorithm from the same article. And I'll just sit on this for a second because it kind of summarizes the way I approach patients that are complex chronic pain patients. I look in my chronic pain assessment, try to apply some of the scales that we went over. Those are those acronyms up there, pain catastrophizing scale, etc. I look at the chronicity. I look at a physical exam. I actually do an exam. I'm also pain-boarded, so I do that part and whatnot, and then look at other comorbidities. Then sort of differentiate between somebody who might have a central sensitization syndrome versus usually neuropathic pain syndrome. We talked about how they're central and nociceptive, but those are rare conditions for a psychiatrist to get involved with. It's usually neuropathic or central sensitization. And then look at, again, the typical analgesics, whether that's NSAIDs, hopefully not opioids, etc. Then TCAs, PTOT, blah, blah, blah. Then the final bubble, atypical antipsychotics if indicated and if there's a comorbidity. If you want to review that, the article is available. The sympathetic modulators I'll just briefly mention are medications that act on the sympathetic nervous system. This includes alpha-active, beta-active agents. There are pain conditions that have significant sympathetic components to it, including reflex sympathetic dystrophy, which is also known as complex regional pain syndrome these days. If you can address the adrenergic component of that condition, maybe some other providers haven't thought of it, you can make a difference for that individual. Maybe you can help them with sleep or with some of the more distressing elements of their pain. Think about a heightened sympathetic nervous system not only manifesting in that focal way of an adrenergic component to a pain syndrome, but also think about whether they're suffering from, again, hyperarousal, hypervigilance, that kind of thing. Propranolol clonidine to sort of make this more manifest can be used for some of these symptoms. This is all off-label, by the way. This is something that you'd have to kind of try with your patient, understanding their blood pressure profile, make sure you're screening for orthostasis, things like that. And of course, prazosin, remember, is used in PTSD. Your patient may be having, and they haven't said this to anyone, they haven't said it to their orthopod, the neurologist, the pain doc, they may be having nightmares about their pain or their ICU stay or whatever, or their car wreck that started their pain. So prazosin may be very helpful. And if you're just helping them get a restorative sleep, you may be already winning half the battle. That's the other thing that I haven't quite highlighted today is that most people with severe chronic disabling pain have really poor sleep. So they have no fighting chance to just jump into PT. They do two sessions and they say, I couldn't do it or I gave up. We need to look at the obstacles to doing PT, whether it's fear, anxiety of movement, or sleep, energy deficits, things like that. Buprenorphine naloxone, as you know, has gained a lot of traction in the world of opioid use disorder or MAT. And there have been a few studies that are a little bit sort of messy that show that maybe there's an analgesic property to this agent. It's not supposed to be very analgesic, right. It's a mixed agonist and antagonist. But some patients report that it helps them with their pain. Now these are all studies using or looking at patients with OUD, opioid use disorder. Maybe we're just addressing their withdrawal. Maybe we're addressing their psychological fear of pain. I don't know. I have seen personally also patients say that I've transitioned over to Suboxone that their pain is better. So take that with a grain of salt. There's a couple of newer studies that are looking at this. One study looked at methadone versus Suboxone and methadone was actually more effective at treating pain, as you would expect. And then another study in cancer patients that looked at transitions to, you know, cancer patients, excuse me, with opioid use disorder that transitioned to Suboxone. And there was a subset of patients who said that the Suboxone is addressing both their cravings and their pain. So I don't know what to make of this. I would say stay tuned. If a patient obviously has OUD, it's already enough of a motivation to put them on Suboxone. Hopefully you can kill two birds with one stone with that agent. As far as ketamine, as you probably are well aware, it's being used more and more in treatment-resistant depression and other psychiatric states. There is actually a very good evidence base for its use in diffuse body pain and complex regional pain syndrome that I mentioned earlier. And the pain anesthesia folks basically use anesthetic doses, stronger doses than we would use in psychiatry with respiratory monitoring, cardiac monitoring, that kind of thing in a specialized suite. So that's where that evidence base comes from. In psychiatry for treatment-resistant depression, it's usually something like 0.5 mg per kg, you know, an infusion for an hour. It's very safe. And hopefully you're helping with depression. The question is, is that dose, that sub-anesthetic dose helping with pain and depression at the same time in people who have both? And the jury is out. One study or one review looked at all the studies and found seven studies that looked at people with chronic pain and depression that received sub-anesthetic ketamine. Three, well, it's listed there. Three had a reduction in both dimensions. Three had a reduction in one or the other. And one didn't respond. So that's not patients. Those are studies. So this is another area that we need more information on. But I suspect that as we get more comfortable with ketamine infusions at sub-anesthetic doses for depression, we're going to see more and more chronic pain patients doing that and or going to pain anesthesia depending on their syndrome. The last section I'm going to focus on and then do a summative kind of statement and then go on to Q&A is the Chronic Pain Rehabilitation Program that I mentioned earlier that I worked at. So the gentleman who was running this before me was a psychiatrist who was facing retirement. He himself had also in a convoluted kind of way fallen into this work. Later himself became pain medicine boarded and addiction boarded. So there's really no neat way of doing this. He convinced me to train with him in this model, applying biopsychosocial care to these complex patients. And basically what it is, as you can see there, they're a multidisciplinary or interdisciplinary treatment model blending all of these things, detox off of controlled substances to remove the barriers we talked about earlier, complex psychopharmacology, medical management of anything else that we had at arm's length, other doctors if needed, if we needed a pain consult or something like that. PT, OT, desensitization profiles, individual therapy and counseling, but also group therapy, biofeedback sessions for coping strategies so that people could be in touch with how their body responds to stress and pain, skills training, et cetera. And then finally family therapy, which is really important for that S of the ABCs of pain psychology, the social stuff. Time and time again we saw the enabling occurring and you could see the light bulb go off and the spouse who was hovering over the patient and actually causing them more harm inadvertently. These programs actually take all. You might think, well, wait a second, this is really reserved for only psychosomatic, functional psychosomatic syndromes. No, there's evidence base actually for failed back surgery syndrome, for really complex pain conditions where other things have not worked. So keep it in mind if you're trying to help somebody with this kind of picture, the various conditions listed there can respond either partially or very effectively to this. Obviously in that modality you're also addressing comorbidities of anxiety, depression, insomnia, PTSD, addiction, et cetera. What's the format? It's basically an intensive outpatient program where somebody's there all day and they're going from activity to activity, Monday through Friday. Then they go home and come back the next day, repeat that for X amount of days. And on certain days extra bells and whistles like family therapy, family education. Significant amount of that neurovalidation education that I was suggesting you guys do in that modality as well. And I'll just mention that at the moment, unfortunately there's not enough of these programs in the country, but there's one in the Cleveland Clinic, there's one at Mayo, one at Hopkins, Stanford, et cetera. So keep your eyes and ears open. You may have a patient who really benefits from this. Even if it's time intensive and everything, remember somebody might have been in chronic pain for 15 years. So if they can do two or three weeks of this kind of care, it might be a game changer for them. In terms of outcomes, those who came in with very high pain disability scores by the time of discharge, you know, within a month later were doing much better. So 93% of them by the time of discharge were doing better on the pain disability index scale that I showed you guys earlier. That does wean with time, unfortunately. So they have to keep up with their practices. This is a change in how they manage their day-to-day pain, right. It's not eradicating the pain necessarily, it's managing it. This is pain intensity, the visual analog scale that we all know, 0-10, et cetera, numeric scale. Those who came in about, I think at 60-some percent, I can't see right now, responded with statistically significant reduction in pain. Notice that not all of them did. This is an important tenet of this. These programs are not promising a reduction in pain necessarily. They're not promising that they're going to have zero pain. They're promising that they're going to have better functioning, the grid on the right. So a lot of this is acceptance work, living with the pain rather than totally succumbing to it and being completely dysfunctional. Change in depression and anxiety scores are there. Depression is the first half and then anxiety. So some response in depression. Notice that anxiety doesn't respond as well. That's that stubborn catastrophizing that we noticed. And some people actually might have even done worse because of the sort of shock and awe of being put through this kind of treatment. So use your judgment. If somebody is so paralyzed by their anxiety, maybe they're not even ready for this. I did want to show this, though, in terms of opioid use. Those who came in on opioids, the dramatic majority of them were relieving without them, either on suboxone or something else. And this is actually a meta-analysis looking at best practices out there or interventions for keeping people off of opioids over time. And I'm proud to say that the arrow is pointing at the fourth line, Huffman. That's our study that we did at our chronic pain program. And it was the largest one with the largest N and all of that that showed that we were very effective at helping people stay off of opioids after that. So that's another perk to those types of programs. If you're going to refer, my advice is that you don't scare them and say, hey, I'm going to send you to some place where you've got to be three to four weeks and this and that. I would advise that you connect them to that area, do a handoff to their intake processes because they know how to talk to patients about this. That's where I learned a lot of this. MI is selling to the patient that, look, you've spent 15 years languishing and you're no better after seeing all these doctors getting all these surgeries, why don't you try this? The intake processes for these settings are skilled at that. So I would advise that they just go for a consult. It can't hurt to get a consult and that's step one. I would use, again, sort of central sensitization, neurovalidation as a stepping stone to help them to bio-validate and to suggest a comprehensive approach to medical, physical, and psychological rehab. Remember all three sort of legs of the stool. And that line that I just sort of spoke about try to contextualize it for them. You know, you're going up and up on your meds. The doctors are referring you to a bunch of dead ends with good intentions, but you're not getting any better. What if we switch it up and do this? In conclusions, because I do want to open it up so that we have time to chat and field some questions, chronic pain is definitely not the same as acute pain. And whenever you see somebody in your office or in a hospital bed or wherever saying, I'm hurting, I'm hurting, they look uncomfortable and they are hurting, you have to simultaneously validate that they are hurting, but suspend the impulse to only treat them with cross-sectional analgesia. Need to contextualize. So consider the central targets when you do that. Consider the actual summative experience, pain experience that the patient is going through. They may not even know. This is sort of pre-conscious work that you're doing, directing them towards something that maybe they can't sit with, a feeling that is really intolerable, difficult. And they may be able to unearth anger, fear, all these various things, depression. Time and time again when I do an eval, let's say I have a 45-minute new eval, time and time again around 30, 35 minutes, these patients are breaking down emotionally because we're talking about these things in a very contextualized way that, quote, no other physician has brought up, right. And that's important to consider in terms of the pain experience. Understand the pathophysiology involved, not just neurobiologically, but also psychologically, and that's where I advise, again, understanding central sensitization, this PTSD pain model, and then of course pain psychology ABCs. Ask yourself, what is the treatment priority right now? If this person is not even getting out of their house because of their pain, is it really analgesia that they need, or is it some kind of fear process that you might want to intervene on? And so that opens you up beyond just Cymbalta, right, or TCAs. Ask yourself, what can I do to help this individual right now? Maybe it's crippling insomnia. Maybe it's something else. Okay. And then of course explore the psychopharmacologic options with creativity and confidence. I would shy away from saying things like, well, we could try this. I would say, unless you haven't done this, but over time as you get experience, I would say, I have seen benefits in this, or the literature shows this. I would use language in a very specific way, because again, these are people that are already traumatized by their pain. They're on pins and needles. They're doubting you as a psychiatrist, and they're listening very intently as to what you're going to offer. And it needs to be jargonized, practical, direct, confident, communicating that kind of competence. And then pair your interventions, of course, with these other interventions. Neurovalidate, that's my neologism that I like to use, the patient. In summary, and in images, I guess, this is a busy one, remember the underpinnings of chronic pain. Remember the pain experience. Ask yourself what's going on at the brain level. Is this person terrified? Ask yourself if I can move them from a basic understanding of pain towards one that is full, and then even further towards one that looks at descending pain pathways and actual neural targets. And then come up with a treatment strategy that integrates medical, physical, and psychological rehabilitation, including meds, which is, I'm under no delusion, that's primarily what we're going to do in this room. And then hopefully, we are at a happy, it's sort of a lukewarm happy. It's not really thrilled, which is, actually, it's very symbolic of what we should be doing in chronic pain, right? We're not going to eradicate pain, right? We're going to be OK with it. So let's hope that you can get there. My references are all listed here. And as mentioned earlier, my slides will be available. So I'll leave it on this slide. Thank you so much. So thank you, Dr. Jimenez, for a comprehensive overview. I do understand where we are on time. And I will have us formally end at noon. But we have time, I think, for a couple of formal questions. And if you're available for a bit after, perhaps, we can have some more informal Q&A, OK? So we'll just start with the room here. Go ahead. Yeah. You talked about the comorbidities. I find a lot of people with GERD, maybe pelvic issues, like hypermetrophy, also fit into that category. And especially in those people, I have difficulty prescribing SSRIs, NSI, because it worsens the acidity issues and stuff. And also, I feel I look a little harder for bipolar mood disorder spectrums. Bipolar, did you say? Bipolar mood disorder spectrums, to see whether if I'm giving antidepressants, it might actually flip them or something. I'm also wondering, I use a lot of quetiapine, small doses of thing, you know? Unfortunately, it is classified as an antipsychotic. I hate it as an antipsychotic. You have to go to like over 400. So it helps them with their sleep, and also, you know, doesn't worsen anything. I think it is a broad spectrum psychotropic, in a way. It does a little bit of everything. Right. Also, I'm wondering if you can speak to the gate theory of pain, you know, where people use counter-intervents, and they hate taking medications. They use a little counter-intervent, so you know, you send some symbols up, and that blocks the pain, you know, signals to the brain. Yeah. Thank you for your comments. Yeah, there's a lot to unpack there. As far as, you know, GI disturbances that don't tolerate SSRIs, SNRIs, or even TCAs, then I do dip into other classes, whether that's anticonvulsants or other, you know, agents. I think you're going to have to be very careful with what you're, you know, managing. Seroquel, on that point, is, you know, the me-too drug, right? Used for so many different scenarios. Yeah, I love Depakote also, like you, you know, common comorbid migraine and mood disorder. So and then, you know, you mentioned many things. As far as the gate theory of pain control, that is the classic, you know, sort of predominant model. And, you know, what I found is that clinically, it's a little inaccessible for patients to understand that. So I don't really use it clinically very much. But it's the way that most pain management docs have been trained, and I would say that it doesn't change my practice terribly much how I sort of select. I look more clinically at what am I observing, and how do I solve a problem for this individual? In fact, I should have mentioned this more during the talk. Being practical with the very first visit with a pain patient is of enormous value, because you're setting a precedent. And then they may follow you into some other, you know, interventions, referrals, things of that sort. So whether it's helping them with sleep, and then now they can do more, that I think is almost more valuable than helping them with the pain initially, so that they can see you past the identity of just a shrink, right, who's going to, you know, psychotherapize me or whatever. I switch a lot of people on presence into good typing, and it takes care of both the nightmares and the sleep issues. So, yeah. Thank you. Yeah. And just so that we can be mindful of everyone's time, what I might do is just stop with the formal comments here so that we can offer you one more round of applause. And then if it's okay, some people can come up and ask questions. Yeah, sure. Awesome. All right. So thank you, Dr. Wenner. Thank you.

Chronic Pain

Psychiatrist

Biopsychosocial Approach

Central Sensitization

Pain Management

Opioids

Anxiety

Hyperalgesia

Allodynia

Alternative Treatments

Patient Functionality

Quality of Life