Get settled, get settled, day two of ClarityCon. Yesterday was so fantastic that I felt like I've become friends with each and every one of you. So I decided I'm not wearing a suit. I'm amongst friends. It's Friday, right? I got to tell you one of my favorite moments of this morning was watching one of you walk in, I don't know where you're at, with a four pack of Red Bull and a Yeti Cup. Now that, that, my friends, is my spirit animal right there. Ready for a full day of learning. Actually, half day of learning and it's Friday. So good morning. Welcome back. I'm Rebecca Helterbrand. I have the pleasure of working at Clarity Child Guidance Center. I hope you enjoyed Dr. Steinberg yesterday. I learned so much from him. Didn't y'all? Big round of applause. And then all those amazing breakout sessions and then Randy Silverman at lunch. What a heart she had for sharing her family's journey. And I don't know who it was that came to ask the question and you made the comment that we learn a lot from books, but it's when people authentically share their human experiences that connects us all. That was the whole purpose of that lunch in yesterday. And we are just thrilled that it came off that way. So just like yesterday, we're going to provide CEUs, the certificates, right after this session and after your next breakout session. So same process as yesterday. If you haven't visited those exhibitors yet, you should. These are great organizations all invested in one form or fashion in the system of care for kids, adolescents, and adults needing mental health services. They're in the lobby. If you haven't gotten those 15 signatures on your passport, you can still do that. We're going to do drawings for free registrations to Clarity Con and Fact. We're going to do one right now. And so I have my trusted friend here, Beth Confer. She's going to stir it with a stick. She's her hand. And she is going to ethically draw one. And I'm just going to announce the name of whoever she picks. We're not looking. And then we're going to pray I can read the handwriting. So we've got Laura Angelo.  Winner, winner chicken dinner. So Laura, if you will take this to one of our esteemed Clarity Con team members, they will get you ready to go for next year. Perfect, perfect. And we'll draw another one tomorrow. So I'm very excited to get those in. OK. So again, surveys to complete after each session today. You exchange those after the session for your certificate. For those of you that are looking for your doctoral licensure, you're going to be looking for the green sheets. So everyone else can use the white sheets on the tables. Doctoral level is using the green sheets to exchange for your certificate. Now, I'd like to thank some very important folks that made this conference possible. Many of you know that Clarity Child Guidance Center is a nonprofit. So as a nonprofit, we do a lot of fundraising. But the goal of this conference is not to make money. The goal of this conference is to give you all the gift of education. And the only way we can do that is through caring sponsors. So I'd like to start with our keynote presentation sponsors, the Greehey Family Foundation, News Star Energy, and Methodist Health Care Ministries of South Texas. And we'd like to thank our presenting title and lunch sponsors for yesterday's excellent lunch with Randy Silverman. Thank you, Community Bible Church. And everyone's favorite grocery store, H-E-B. A full listing of all the wonderful sponsors that made this possible, including the scholarships that many of you are using right now, is in your syllabus. And now, I'd like to introduce this morning's keynote speaker, Dr. Dan Matthews. Dr. Matthews is the Corporate Director of Neuropsychiatric Services at Neurobehavioral Systems, the Division of Universal Health Services, Inc. He obtained his medical degree from the University of Texas Medical Branch in Galveston. Dr. Matthews specializes in child and adolescent neuropsychiatry. He has published widely on topics relating to the assessment and treatment of pathologically aggressive youth. He served on the faculty at the Duke University School of Medicine, where he was the consultant to state programs under the Willie M. Federal Class Action suit, treating adolescents who exhibited violent behavior. His research into specialized assessments and medical stabilization of pathological aggression has led to his procedures becoming a standard of care nationwide. Dr. Matthews has been medical director of several neuropsychiatric facilities in Texas and is consulted on the development of other programs nationally. He provides supervision and training for the neuropsychiatric programs at the Maradell Achievement Center in Austin and continues to do research on the effective treatment of brain disorders in children and adolescents. He regularly lectures on topics in pediatric neuropsychiatry for clinical professionals. Please join me in welcoming Dr. Dan Matthews. Thank you very much. Yes, I think basically my entire career of well over 30 years has been impulsive explosive aggression. And the work that I did at Duke when I was on the faculty there was found the answers to that. It was in conjunction with the pediatric neurology department at Harvard, and we developed a mapping system, an electrophysiologic mapping system that allowed us to look at deep brain difficulties without actually penetrating the brain, which is a good thing. Some of my staff would have loved to have these brains penetrated, but that's OK. Oh, OK. That OK? That better? OK, I didn't want to hurt anyone's ears. I can get pretty loud. We'll take that away. That way I don't have an echo. All right, so basically what we're going to talk about today is a new diagnosis in DSM-5, disruptive mood dysregulation disorder, which will henceforth be DMDD, OK? Because I don't want to have to keep saying that over and over again.  It is recognized in the ICD-10, came out in 2013 in the DSM-5. And the research that I'll be talking about is really, part of it is we do outcome studies on every patient that we treat. And we follow them at one month, six months in a year. The outcome studies, so that you have a frame of reference, essentially the medications they went out on or listed in terms of dosage, frequency, et cetera, at the top. And then there's a question, if anything has changed, please put this information in in the next rank. And then below that, the reason for the change, which is either side effects, inadequate effectiveness, or position choice. So basically, 85% of the time if it's changed from what we had them stabilized on, it's position choice. It's not that it's ineffective. It's not that there are side effects. And it's not refusal by the patient or the family. So we do great efforts to educate people that are receiving the patients about what we're doing, why we use these medications, because they're different. And what the effectiveness is, how they work, et cetera. And we actually mail out to physicians receiving the patients a folder, which actually has research references, our research, research, and as a result, we have managed to decrease the non-compliance, which is changing the medication to probably less than 20%, where originally it was 50-50 whether they would stay on it or not. And when we talk about the outcome studies, which I will show you, and we do them, we've been doing them since 1991, and they've been peer-reviewed and published over and over again. And so basically, we don't try to publish them all the time, because my colleagues at the American Neuroscied or the Association get a little bored with that, because the outcomes are almost always the same. But it's a comparison between leaving the medications that the patient was stabilized on at discharge in place or not, and the difference is an outcome. So we'll talk about that. Disruptive mood dysregulation disorder we will also talk about in terms of behavioral management as well as medication management.  It's in the limbic system and the emotional brain. It is constantly surveying everything and making decisions of what is a threat, what is not a threat, do you fight, do you flee. In rabbits, they can also freeze, but that doesn't work well for them. If they're threatened and they freeze, that's not good. But anyway, and these individuals, their fight-or-flight system is about the same level as if they were actually deployed in Afghanistan. It's four to six times baseline, but it should be. And that's at no stimulizer than just click-click or flash-flash. It's not scary faces, angry faces, anything like that, that you can certainly generate a big response from these individuals on FM functional MRI. But essentially at that level, they are hyper-alert, hyper-focused, constantly feeling a threat. They don't know why they feel a threat, but they constantly feel threatened. And in many circumstances, they have been abused other things have happened that they would feel threatened in certain circumstances, but it's exacerbating. And with the DMDD, basically they have two things that are critical. One is excessive fight-or-flight system at baseline. The other is inadequate brakes to control it. A dysfunction in the frontal lobes, which is the feedback system to stop the expression of the aggression is inadequate. So you need to address both of those and I'll show you what that looks like in terms of neurophysiology and so forth. I'll keep it where all of us, including myself, can understand this. But basically it's very straightforward and with that we will begin, okay? Ah, not turned on. And this occurs where? We're saving battery. Thank you. That is the contact information. It's on all the slides are there. I noticed one thing we're going through all of my slides will also be on Clarity's website. And you can access the real pre-colors instead of just the black and white. But you've got something to take notes on that makes sense. I have to, as a physician, indicate medication usage disclaimer. There are two medications that you will hear about in treatment today that are not approved by the FDA for use in children for explosive aggression. Be aware, however, that other than two of the anti-psychotics that are used massively, only those two are actually approved for use in children by the FDA for aggression. That would be a vilify and a spare at all. And just for aggression in autism, nothing else. So in Charles' country, now there have been laws passed that say you have to, if you find something, you also have to apply that in children and you have to do the same research to get it approved. In the past, what we would do is just translate, okay, that works in adults who have tried in children that look the same. So there's not good research. There's getting to be more and more good research, but right now there's not that much replicated research on different medications in children that seem to work in adults. So everything is off-label, basically, with the exception of a couple of things. There are, after all, at least 20 second generation anti-psychotics, so 10% of those are approved for aggression, all 20 are being used for it. So, and I will tell, I will reveal the names of these two secret things shortly. But they are key to our success. Okay, disruptive mood dysregulation, I said it again, but that's it. I'm really gonna stay with the DMDD. We can say probably 15 minutes of this talk if we don't say that over and over. How does it compare to severe mood dysregulation, which is actually a research diagnosis from NIMH, Severe Mood Disorders Group? So it's not a DSM diagnosis, but it's the same thing in adults, because once you turn 18, you're cured. Just like once you turn 18, now you can be a borderline. Once you're 18, you no longer can be DMDD because that's a childhood diagnosis, which is part of that, and I don't wanna be too disparaging a DSM, but it's done by committees. Just be aware, as you see some of these diagnostic criteria, you've got 20 guys sitting around, or men and women, depending on how long they've been doing this. But bottom line is, for instance, one of the criteria for DMDD is that they have to have had, on average, three explosive rage episodes a week for a year. Now how many of these parents are gonna be, that's one, that's two, or you can't make the diagnosis until you can't treat them for that diagnosis, and if the parents survive while they're doing this, and don't repress it totally because they're so traumatized by it, you're never gonna get those numbers, and I know how it works, because I sat on some of those committees and I quit doing it, because it's kind of a kumbaya thing. I think it should be five. I think it should be one. How about two, four, three. Hey, we're gonna have beer, okay? And same kumbaya, we solved one more problem. Yes, there's no science to it, can we all just get along? Well, we can get along with three, except the rest of us out here is trying to get that count from somebody, and it can't start until six, so that you've ruled out the normal temper tantrums, but it has to be diagnosis before 10, so you've got four years to diagnose them, while nobody's counting three a week, three a week, three a week, you know? And it's just, so it's difficult, you can apply these things retrospectively, and but you're never gonna have that documentation of three times a week for a year. It just, I don't know why they thought of that, other than they just didn't want to diagnose it. However, retrospective research that we will talk about has actually found applying in mental health consumers, children, not the general population, but those who are actually in treatment for mental health disorders, as opposed to the previous 4% who were bipolar disorder, three of each of that 4% are DMDD. The bipolar is back down to 1%, where it was before all this started. There was a 40-fold increase in the last 10, 15 years of the diagnosis of childhood bipolar disorder. Excuse me. So, I will show you, all of these references are in the back, that's why that's such a big packet, because there's probably 17 pages of references.  But bottom line is, it is well-referenced. And we will be talking about the neuropathology. Yes, all children are irritable at times, when you don't let them have what they want, they're irritable. We, as adults, are irritable if we don't give what we want. We can cover it up a little bit more, but it's not even on the face, it's kind of a giveaway. I'm not happy. Temper outbursts three times a week. Almost daily for a year, again, irritable, angry moods. So, you know, they're just basically saying, until one year after six, that you have all this documentation, you can't make this diagnosis. Now, on the other hand, you can make childhood bipolar diagnosis without any episodic changes in irritability. So, you know, it's all, and it's not even, never made the official diagnostic carriage noise. They do clearly have trouble in multiple settings, and as we mentioned, there's a age range, but when it can't happen, and once it does, you gotta hurry. Because you can do that retrospectively, because it's still going on after six. Most of the time, it's been going on since 3, 4, 5. You just can't count those years. At least the ones that we see, who have, when you look at these outcomes studies, to be aware, they have had 3.5 previous incarcerations or hospitalizations for aggression before we see them, which we do not require. It just kind of works out that way. And that's been true for the last 25 years. Yeah, briefly, designed to replace the broad spectrum childhood bipolar disorder. And this was a conscious decision on the part, because various people have already published, Layton Luth, whose name you'll see over and over, who is the head of severe mood disorders, is that there is no such thing as childhood bipolar disorder without episodic irritability. So you can't make chronic episodic unless you just turned your back and you didn't see it right then, then it turned around and there it was. See, that's episodic. 1990, 10-year period, 94 to 2003, there was a 40-fold increase in bipolar disorder in children. Now, other than eubonic plague in the distant past, mankind has never been struck by that severe an epidemic of something. And it's not viral, and it's not bacterial, it's not fungal, it's diagnostic, basically. So it's, now we're gonna go back down to where it used to be. And I'll show you some of the genetic studies, some of the other things that indicate why these two things are so different, because the neuropathology is totally different, the neurological reactions are totally different, the family history of genetics are totally different, the brain mapping in the other, brain mapping besides our is totally different between bipolar and these, so they're two different things, not one lump. The key piece, and I won't repeat this over and over in the slides, but basically, they're not classic, they show non-episodic chronic irritability, not constant, but virtually constant.  And basically, we're gonna be doing some research with UT looking at on some of our kids with tractography, do the white matter tracks have deficiencies, or is it just the dopamine receptors in the frontal lobes? I think probably there's gonna be some of both, so that's the cable wiring, it's sort of like, if there's broken pieces in your cable, then you gotta get a time-warner or somebody out there and fix it. If you change the stimulation coming through there, it actually will increase in size again. That's known as essentially a genetic alteration, an increase in actual work of that particular gene, because now there's a demand. We need more receptors. You have inadequately more receptors.  It's not like it's there permanently. When I trained, basically, I trained in neurology, child neurology, psychiatry, child psychiatry, and I was also trained in psychoanalysis because I was trained in the late 60s and early 70s. Not that I show that, but hey, I've had work done, okay? Really just replacing two knees and a hip and a few things like that. So in essence, we have to get away from the idea that back then, because we had to rotate on neurosurgery, we had to teach neuroanatomy in addition to all the other things we were doing, but they insisted that we knew brains inside out from what we knew at that point. And so in essence, we've got to recognize, because back then it was like, you know, if you lose the function of something, you're done. You know, it can't be changed. It can be changed. There are stem cells constantly being produced by the hippocampus, particularly in other areas of the brain as well, that go to different areas and they are showing up as a ubiquitously available cell. And then they fill in, because that's how you change in child and adolescent times as we get older, we change sort of, not so positively, we sort of go backwards, but at that point they're shifting and they say, we don't really need this bunch of this function anymore, we're gonna take this away and we're gonna do this instead. It's like, you know, except for brilliant individuals, you don't try to teach algebra in the second or third grade because they don't have the capability to do that. It's always held until they get into puberty and then they start changing into more frontal lobe function. And of course, as you know, males' frontal lobes are a bit slow in comparison, but we do catch up kinda somewhere in the mid-20s. So basically, all of these things are amalgamable now. So even the vulnerabilities that you bring to the table, if you're treating them the right way, stimulating them the right way, putting them in a situation where they now are functioning the way they should, even though it's artificial, at some point about 50% of these people go to normal and they can come off the medication. That does not happen in bipolar. And I'll show you the statistics, but basically, you know, virtually none of these children in long-term follow-up now that they've re-diagnosed them this way and then looked at where they are all the way up to adolescence and adulthood, particularly in Sweden and other places where they got everybody's medical records, they can retrospectively look and go forward and do whatever. And they've done some fantastic studies, but they basically say they don't become bipolar. So, which is good because that's chronic incurable, like type 1 diabetes. At this point, it's incurable. So it's a mix of genetics that's different than the mix of genetics in these individuals. 1.2, I think it's correct, we'll see in a minute, 1.2% of these individuals have bipolar parents versus 30% of true bipolar children. So all the genetics are different. Everything is different. Okay. Essentially, again, not to beat it, but it's non-episodic versus episodic. There's no psychosis involved in this. This is Dijkstein and Levenworth in 2012. Let me go back and watch. No, I'm done. Okay. Yeah, essentially that's the adult version of the same thing. And they did research and they showed that anti-psychotics are not helpful for the severe mood dysregulation other than sedating them. And so they do not recommend it. Chronic, severe, childhood onset, and so forth. But basically, the severe episodic irritability is symptomatic of a manic phase. If it's episodic, if it's not, then it's not manic. So you don't get credit. Yes, sir. Just so everybody can hear. Because I'm screaming. I'm sorry, I was just saying. We're gonna do this routinely. We will do Q and A in the last 15 minutes. Okay, I'm sorry. That's fine, go ahead. I was just thinking, a supervisor I had one time said that he wouldn't diagnose bipolar disorder in kids, particularly adolescents, if there's not a history of pressured speech and grandiosity. Yeah, well it depends on the eyes of a holder.  Could be pressured speech, just putting pressure on me and bothering me. There's a difference in the terms of the pressure. And so all of those, just real quickly, most all psychiatric diagnoses are in the eye of the beholder. We proposed that in DSM 3, 4, 4TR and 5, why don't you diagnose this as limbic dysmodulation disorder, because that's what it is. You have an emotional brain that is out of control and there's no modulators. Then you know what you're gonna treat. Otherwise, you know, right now the basically from the NIMH has come the research diagnostic criteria which is really a neuropsychiatric approach. Essentially, I do not want to fund any longer treatment of paranoid schizophrenia. There are 10 symptoms. Which one do you wanna treat? And you pick one and I don't care if you're sure they qualify, but I want you to know, I wanna know what that symptom is that is disabling, which frequently as you know, crosses over numerous diagnoses. And then I want you to map the brain. I want you to propose to me where in the brain you think this symptom is being generated. Because it's not coming from the liver folks, okay? It's coming from the brain. So let's then look at that. We've got excellent mapping of all kinds to look at all these things. We can look down to neurons connecting at this point and see if that's dysfunctional. I don't care if it shows up on MRI as a lesion or what, generally there's no lesion. There's nothing that we find even with four Tesla MRIs and just think about one Tesla that's the strength of the magnetic field. One that can pull your teeth out of about four times if you got any braces on or anything else. But those things cost about a million dollars a Tesla. And you can look down to the cellular level with them. But at some point you get so much information it becomes confusing. It's sort of like when you put 128 electrodes in a net on somebody, they're not that far apart. So at some point the gain is really not worth it because you're just looking at a jumble of information. So basically we need to map it, show that it's dysfunctional. Now tell me a chemical slash drug that you think is going to improve that dysfunction. And then apply said chemical to the individual. Measure the symptom. If the symptom improves you're halfway there. Now re-map it and see if the actual dysfunction has been improved. Now we can go looking at the genetics that we think might be doing this. Now we can look at primary or secondary prevention versus tertiary prevention which most of us get because the train wreck is already done. So you're just trying to save what pieces you can. So anyway that's the approach that needs to be done. That we've spent, according to the people that I know we've spent billions of dollars doing all kinds of research and we can't replicate each other stuff. Just like with ADHD, you get one group that finds excessive abnormalities in dopamine D4 genetics in the frontal lobe. And or not in the frontal lobe in ADHD generically. Others find D2 abnormalities. And the difference is that the D4 is abnormal in the frontal lobe. The D2 is abnormal in the hippocampus which is the attentional system. And you got five symptoms each that are attentional or impulse control, concentration, et cetera. And so somebody gets more of this, somebody gets more of that, somebody gets equal amount. That means that they're hippocampus and their frontal lobe is not functioning. But they can't replicate each other so you can't get replicated research because you don't have to keep a list of which five you use. You need to pick five of their frontal lobe and then test. Somebody else needs to pick five that are gonna be attentional, hippocampal and test. Not some mishmatch of the two. And it's just, they've never been forced to do it. So it's now the funding's just not gonna be there unless you do it. Okay, back to DM, I can see this one better. I'm not ignoring people there. I'm paying attention over there but I have to lean out further to see that one. Basically, that's just speak for itself essentially. Epidemiologic, this is Copland, the other studies that I'm talking about also, you'll hear about dotery. Essentially, they found anywhere from 3% of the mental health treatment population, the whole population, the 3% of those in treatment, and they were in outpatient treatment in various, it's multiple, just multiple areas. And what they found was at least 3% met DMD criteria retrospectively. I'm pretty sure they probably ignored the one year thing. I didn't ask them because I've done retrospective research and that's what you're gonna see here although we're doing prospective now because we get to kids that you know they've been doing this three times a week for a year even if parents can't remember it, they just remember that it seems like forever and it never has stopped except when they're sort of stoned. So basically, this dotery found 8.2%. So it's somewhere between three and 8.2 and he was really just looking at six-year-old children who were chronically irritable and explosive. So my guess is it's three or 4% of the population. And we got, just as an aside, we frequently, we do some outpatient stuff but most of it's inpatient and basically we would do outpatient mapping and make recommendations if they don't need inpatient but the bottom line is that we get called here the last year or so when the DMDD really got rolling that they went to one or another academic center with their bipolar child at seven or eight or nine years old and they said, and had been under treatment with antipsychotics, et cetera, since age four or five and basically they were told, no, your child is not bipolar. Your child has DMDD. Thank God. What do we treat with? We don't know. What does that mean?   I said, well, if their DMDD will map them, we'll show this and then we'll refer them back to the academic center. Well, they went back to the academic center and they said, you know, we don't agree with that. So we haven't heard of those medications being used. So bottom line then, they may find a psychiatrist in the community and we know who's who all over the country in terms of who's complied and who's not because we get the names as they send back the information and that allows us then to give them other choices within the community depending on their payor and the payors wanna know who's on our panel that actually does this so we don't see Johnny every other six months back in the hospital again. It's not altruistic on the part of the payer it's financial. Doesn't make sense to be paying over and over again. So basically, probably to an extent, they end up with depressive disorders as they followed them in late adolescence or early adulthood, but they do not become bipolar. They don't become bipolar. And they also 85% have comorbid ADHD, shock and awe. Part of that is because their frontal lobes don't function but also they have dysfunction within the hippocampus as well. So here we have all the different findings of different researchers, all of which are listed there. So you end up with kind of a 4% somewhere between the extremes, many coexisting. There's the criteria. And basically they meet those beyond provocation, not consistent with a developmental age six plus on set before age 10, never elevated mood or grandiosity. That's again in the eye of the beholder. Well, I saw them, they were happy. They must have been insane, their life is miserable. Now they need an anti-psychotic because they've gone crazy because nobody wants to be around them. They can't control themselves, not one, it can't. In the schools and everybody else, think everything's volitional. They'd probably tell people, if you just quit having grand mal seizures, life would be a lot better for you. This is a seizure equivalent basically within the limbic system. When it goes, it goes and they're not there anymore.  Really you're not but that is what their mindset is. Mood, chronically irritable, angry, negative. Something like some people I know. It's like, hey, don't worry, be happy. Go to Colorado, the happy stuff there or otherwise. By the way, marijuana or cannabinoids are good for limbic dysfunction. Let's move it out. But the thing is that chronically using it, it blocks the development of stem cells in the hippocampus.  I'll show you a picture in a minute. It now looks like when you come out from the aquarium and you want to get a souvenir seahorse, it's a dried up little thing and if you drop it, it breaks. That's the changes. It actually shrinks over time. That's memory filing problems, that's attention problems, that's true. So it's not Norovoco and others at the drug area of NIMH or coming out with all the research that's been there. The chronic use of this stuff is not a good idea and what we've got now, because if we look back when some of us might have imbibed in that in the 60s and 70s, what we've got now is 10 times more effective, 10 times more powerful between the growing and then the concentration and the other kinds of things. At least 10 times what you may have been exposed to 20 or 30 years ago. And that's just gonna make it that much quicker. I went to UT and then the medical school, UT medical school down in Galveston and I was a jock when I was at UT. And so I go, you know, when I was in medical school, I'd come back and go in the drag and some of the same people were there that you were in school with. And you come back 10 years later and they're still there. And how's it going? Ah, a couple more classes and I'll be done. And basically their parents were just keeping them there so they don't come back into town and embarrass the hell out of them, you know. There's nothing going on there whatsoever, you know. You remember when? Oh, well, hey, how's it, those classes going well for you? Yeah, as far as I know, seems okay, you know. So it's, reunions were kind of strange sometimes. Kind of like bumper cars. Boop, boop, boop, boop, boop, boop, boop. Who are you? I don't know. So basically those criteria are stringent to say the least and they've been stretched beyond rationality, quite honestly. I think partly because they were just dipping a toe in to see if the alligator would jump up and get them because they were challenging bipolar disorder. Think about the number of publications of treatment of childhood bipolar disorder that have underpinned numerous academic advancement, et cetera, et cetera.  A lot of powerful people that weigh up here and they're experts in childhood bipolar. Some of them have now become experts the last time I talked to them in intractable childhood depression. They don't talk about bipolar anymore, which I thought was intriguing. Probably they can empathize with intractable depression because never mind. I'm gonna get myself in trouble, which I frequently do. So I gotta go this way, I can see it better. I need to see what I'm telling you guys about it. I can make up all kinds of stuff but it's probably better if I stick with it. We were some of the first ones to look at it is what's the genetics of something that we at that point is called intermittent explosive disorder. And again, we found D4 abnormalities and D2 abnormalities. And so we proceeded then to address the D4 abnormalities with amantidine hydrochloride and then once we could stabilize the amygdala with the mood-stabilizing anti-convulsant, all of this will be revealed before the day is over. The actual names, generically, because they're all generic. Then we could put in a stimulant and stimulate the hippocampus to attend better and we treated all three of the problems. If you put the stimulant in first, they just become more explosive, sort of like taking somebody to a disco with strobe lights when they've got poorly controlled grandma. They're gonna look different on the dance floor pretty quickly. These kids, they can't, they got ADHD but they can't have stimulants because it makes them irritable and explosive. They don't make the ADHD go away, they still have ADHD. So, and you'll see the Fisher-Matthews name over and over again. Genetic disorder to an extent, yes, sometimes you need also additional hypoxia, drugs and alcohol and pregnancy, which is fetal alcohol spectrum now and Amantadine works wonderfully for that because it's a frontal lobe dysfunction. Difficult birth, malnutrition, abuse, all the above. They can all be there. There are lots of people, probably 25, 30% of our population is adopted and people who impulsively become pregnant or impregnate, because it's a joint venture, then have significant drug problems, don't have any prenatal care, et cetera, et cetera. And we've had parents come in, adopted from a Russian orphanage. The mother was a college student and the father was a mid-level professor at the university, go by it. So this child, and it's been a while, nobody's adopted them, so they've been laying in a crib for a year, year and a half with sensory deprivation, flip them over, it's kind of like a spatula. And if you just love them enough, it's gonna be okay.  So you don't care about them, you're not touching them, trust me, I care about them, I don't know what's gonna happen if I touch them. And so over time, it's sort of a con job, really, that many adoptive agencies, they're reaching out all over the place. Chinese children are excellent, particularly Chinese girls, because they're just not wanted, they can't stay there, they gotta go somewhere. So they don't have that same deprivation, intoxication kind of background. Bipolar, this is just some of the differences. Bipolar rates do not vary by gender, but chronic irritability, shock and awe, 66% male, two-thirds to one-third female. Distinct gender-based disorder, parents of Bipolar should 33% are likely to be Bipolar one or two, both, I mean, one or the other of them. Of course, it's 2.7%, so it's 10 times greater than 10 times more likely that they're gonna have Bipolar parents. So again, it looks like a genetic disorder. Gene mapping will help, but we're gonna, it's getting better and better, but it's also, all of these disorders are not like Huntington's where it's one gene, one disorder, it's a dominant, oh God, one gene, one disorder. It's gonna be multiple genes interacting with the good or the bad one way or the other brought into the mix, which could never happen with a straight A college student and a college professor reproducing, you know, there's gotta be good genes across the board, not. Cause that's not who was reproducing. There's no established treatment strategy. Bipolar medications may not be needed. We've demonstrated that in some of the research that you'll see in there. Selection of medications management is difficult, no matter who says it, Kovach, us, others, Sermos, Abios, it's hard. It ain't easy, but it becomes very easy when you find what works and what doesn't impair other functions. Step one, do no harm. That's what medicine talks about. Medication, parent therapy, psychotherapy, all of which are good, but without medication, it's gonna markedly decrease the benefit that they get from any kind of other therapies or behavior therapy or anything because it can't behave. And they only see it as a threatening process.     And then you become diagnosed, which is not really, should never be a psychiatric diagnosis. Opposition of the fight disorder.  Oh, well, you have opposition of the fight disorder. That'll be 20 days in the bread. That'll fix that. There's nobody else knows. There's no medication that fixes it. What fixes it is taking care of the underlying disability that they're trying to protect. You're telling them, you know, count to 10. They can't get past three. It's a great plan for anger management, but they don't have the capability. It's sort of like walking in the room and everybody's sitting in a chair and then everybody stands up and one person doesn't. And they say, why didn't you stand up?  Is it not obvious to you that I can't without assistance? So basically, you know, you gotta look at it that way. Everybody, my view is that everybody wants to be successful. Everybody wants to do well. If they haven't, they give up on it. Then, you know, in adolescence, then they may switch over and decide just be, all I've been is bad, so I'm just gonna be good at being bad.  They can't lay it white and lark on somebody. They just, you know, snatch something to run or whatever in front of the cop, you know. So the gangs don't like them unless they need them for a distraction down the other corner while they're gonna do what they planned and organize today. So they can't be successful in a career of crime nor in a career of doing well. They can't do those things. They ain't got any skills that will do it, but the skills can come if you make the brain now available to do it. But they're gonna be behind because everybody else is making the developmental steps as they go and these kids have been stumbling, falling off the road and so forth for years. So it takes time and it takes patience, but you can see it happen. We can see it happen at a rapid pace in the inpatient setting when we have them because we're doing all of these things when we know they can do it and they suddenly find out they can. They're not great at it but they find out they can and then they really invest in it. Otherwise they invest in, I ain't gonna do it. But I'm gonna be embarrassed. The principal's office, why did you, you know, Johnny, you knew what was gonna happen when you did that, right? Yeah, why did you do it? I don't know. Well, if you got no breaks and you got the impulse, then it's already in action. Oh God, I've done it again. After a while you start blinding everybody else. And to an extent, that's true because you expect me to do something I can't do. But they don't know they can't do it. Well, they know they can't do it but they don't know why they can't do it. So, and this Aemon is not the same as Dan Aemon. Okay, I know Dan and this is a different Aemon. Medication protocol. Your psychiatric approach basically shows neurophysiology is abnormal. Symptoms come from these areas. We're going to treat this. And then you do that. You've got underlying basic evidence that these areas are dysfunctional that you propose would be dysfunctional to resent this kind of picture. So it's a top-down bottom-up approach. Bottom-up is this 800-horsepower engine that's running the amygdala, the fight-or-flight system in the brain. And top-down is the brakes which are not functioning. So we've got to fix both. Fixing one helps, fixing the other one helps, but it doesn't give you 85, 90% elimination of what's going on. This is an angry child. This child is frustrated by you're not letting them have something that they want or do what they want or whatever.  You can see the cold eyes. I'm going to get you later. And I'm going to bring three of my friends and we're going to jump you in the play order. We're going to jump you when you're going to your car teacher, we're going to do something. We're going to get you. And then you'll learn that next time I get to do what I want to do. I can't fix that. That's just plain mean. I can show you in brain mapping what happens in the emotional brain that these individuals at rest, their reactivity to just click click or flash flash is 50% of the normal. They have at the same time, if you do a startle reflex, you just episodically puff air in their eyes. They have a decreased auto reflex. They have decreased basal heart rate, but they're not slow. They just are decreased in reactivity. They have decreased feeling of pain. They are psychopaths. And that's a whole different thing.  And they wanted to know, given my research, because they'd already done galvanic skin response, which basically is a lie detector test. You sweat under pressure or you don't. They don't sweat. They can pass lie detector test because they don't feel any pressure. They don't feel anxiety. So in essence, they want to know if we would look at the deep brain function of these individuals proposing that their limbic system is under reactive. So I said, well, with this caveat, none of my people nor I will be known to any of these people because they're free range in the community. I think you guys are nuts, but you've got a group and we're gonna do them. You say we're gonna do, we've got another test we wanna do and they're fine with that because they're coming out of prison. I mean, it gives them a chance, you know. So basically what we found was 50% or less of the same responsibility. So, basically, this can get me in trouble. Somebody said, what would you do to improve that? I'd do what they do. I'd make sure that they had an extra amount of cocaine every day and we did blood levels to be sure that we were stimulating this area. Well, our kids, if you put them on cocaine, they just explode, you know, because it's enhancing that same reactivity. It's increasing it. So, I didn't publish that. This is range. This is a kid that you do not touch. This is a junkyard adult. He is protecting himself, his territory, his eyes are glazed. If you look at pictures of dogs barking and they have the same pulled back teeth showing, cats do the same thing. They show teeth, they fluff up, so they look bigger, et cetera, et cetera. They're trying to intimidate.  And they're basically, like I said, operating as if they're in Afghanistan. Basically, own deployment. Everything is dangerous. So their heightened alertness makes them more likely to go off at the least minor crossing of them. Okay, these are the incarceration, these are several different years, all of which have been peer reviewed and published, compliant, stayed on the medication, non-compliant, somebody changed something. 1%, this is an incarceration, 1% versus 18%. Rehospitalization for aggression, 5%, within one year versus 40%. 58% versus 6%. 10 times as likely. The scary thing is, this is another year, subsequent to that year, one year post again, incarceration, 0% versus 19%. You can't make this stuff up, guys. Okay, re-hospitalization, 6% versus 48%, so 67% versus 6%. I've been seeing this for over 25 years. It repeats itself, that's part of why we don't publish it very often, about once every five, six years, just to remind everybody. Because it's, you know, the nearest contrast, that founding member of ANPA, American Neuropsychiatric Association, look at that and say, yeah, well, of course. This is treating the underlying problem, and that isn't.  It's always a different year, a different group. We have data on several hundred patients every year. But it's, to me, you know, it's actually, the thing is that the compliant group is consistently increasing, and the non-compliant is decreasing, and it will reach a point where it's not gonna be statistically significant between the two. At which point, I'll be just happy as I can be. But I have seen a difference in results when we get more information to them. If you've got somebody on amantadine, amantadine is used, basically, it was used to treat Parkinsonism. It's a dopaminergic activity. It's also been used in children to treat Type A flu and prevent Type A flu. There's been resistance to Type A flu that developed resistance to it. But people will say that, you know, doctors say, well, what have you got amantadine for? It's not flu season.  And it's gone. All right, brain. Basically, three key pieces. And I don't think that'll go from here, but I'll go both sides as I walk back and forth. Just don't let me get so distracted that I fall off. Okay? I tend to really get into brains. All right, basically, what you're looking at here, this bluish purple is the hippocampus, which is Greek for seahorse. This area is the amygdala, which is Greek for almond. That's the fight-or-flight system. This is the, both of these generate emotions. They're very intimately connected, as you will see. Maybe one in the middle, then we can all share. But I guess nobody wants to share. Okay, so basically, yeah, it's going, you can see it all at one time here. Actually, those are measured in milliseconds. I can't go that fast, but okay. All right, stop, stop. Okay, all right, I got this. I'm just having way too much fun. And hopefully nobody's about to have a seizure with this. Okay, must have worn out my battery. Shit. Turn my back for just a minute and look at that. Very carefully then. There is the hippocampus and the amygdala, intimate connection between the two. This is the fight-or-flight system. It's constantly getting into it from outside, inside. Something's not right. You need to do something. I don't know what it is, but you need to be ready to do something. Something's not right.  Something ain't right here. I don't, you know, I need to be alert to this because if somebody, snipers are here or something is here, you can just feel it sometimes. Sometimes you over-feel it and everything seems like probably I shouldn't be here, which is the real message that's being sent. How are you doing?  What are you thinking? Not. So then it goes, and I'll be right back over there. It all feeds into this system right here, which is the cingulate gyro. The back end of this is just conveying it. When you get right in here at the bend, it starts trying to control the intensity of what's being sent forward. Oftentimes to no avail, but it's trying. If it's working normally, it's gonna begin to damp that response so that it comes down to here. And then at this point, it's sent into the orbiter frontal, which is right above the eyes. And this is the final braking system. Stop. I know that someone provoked you, but we need to check out this situation. So I'll show you the same pieces over here. At least what I said I would. I'm afraid to put it down because it's there. Essentially, we're now moving into the cingulate gyros here, the primitive gray cell, gray matter. And then it drops down to here, the control start at this. This is known as the knee of the corpus callosum, the connections between both hemispheres. So it's knee is genuous. So it's subgenual. So you get all these terms right, okay? So it's turning the corner and it's fixing to drop off this package that it's sort of muted down to some extent into this area, which is the orbiter frontal. In terms of my psychoanalytic training, the limbic system is the id, particularly the hippocampus and the amygdala. And then the transmitter is there and when you get to the orbiter frontal, it's the superego. It's sort of like the devil angel, are you? He said something that I need to kick his butt. Okay, I know you do. Your man's gotta do what a man's gotta do, but let's see what the odds are. Just hold it there for a minute. Then it goes to big brother up here, the frontal area. And that is the ego. I've trained so long ago, we had to call it ego and superego. Now, if I talk about ego now, people are gonna be totally distracted. We had to be classical though. So in essence, this frontal area is now saying, okay, I'm getting information that you're really angry. And the information says that you've been provoked. And I've scanned outside of here. This guy's twice your size and has a baseball bat. Per chance, we should rethink our strategy. Okay, so he retreats from the field, goes and gets his brother, comes back with two baseball bats and beats the hell out of the other guy. Otherwise, if he just goes in there because there's too much saying you gotta do something now and not enough whoa, at that point, he gets hit between the eyes with a baseball bat. And when he gains consciousness, none of those brain pieces work better. It's not an improvement. And if he does it often enough, he gets chronic and cephalopathy and he really has no control. So what we find, this is, I had done just for me, this is the limbic system with everything carved out. Again, you gotta get to be first this time. We'll try to see if we can stay right here till we can get through with this. So this is the hippocampus. This is the cingulate gyrus. And this is the genus.  But basically, then this is the amygdala. And notice how intensely they're connected and then they consistently connect back into this system all the way around. So this is being reinforced all the way through while they're trying to be controlled once it gets over here. So bear in mind that just as an aside for functional purposes, again, the hippocampus, the amygdala, the posterior, medial, anterior subgenual cingulate. And pretty much this is classic. There is no over-the-frontal there. There is in these individuals. You don't see it fronting, you don't see anything else. It's just not working right. And so basically, just note the alfactory nerves. They are, these bulbs are just right behind your nose. They gather all the scents and so forth. Note that they're directly connected to the amygdala first. This is why we snore cocaine instead of swallowing it because it goes straight to the limbic system, which is where we're trying to get it to. It doesn't get wasted throughout the other 98 or 99% of the body fluids. And the problem is if you do that, then you're gonna stimulate an amygdala that's already fired up and then you don't get to come back to the party next time because you beat everybody up, okay? Okay, this is what the caps look like. This is basically one of the people that's been set up to have a cognitive race, which is a complex EEG with a bulk potential. It's 32 leads, not 128. We don't need that many. And this is an auditory of bulk response. We're looking at 32 of these on each electrode. We know which electrode it is, the 15-year-old right-handed male. Basically, we have male, female, right-handed, left-handed age ranges all the way from infancy now because the guys at Harvard have continued to go all the way back to infancy with normal groups and all the way up to age 80. After age 80, we give up. Yes, ma'am, we're gonna need a microphone somewhere. It is, part of it is a QEEG. We do, yeah, it's just additional testing on top of that. QEEG and the spectral analysis are useful, but they're not particularly useful for us because they're not that different in these individuals compared to the normal. And so we kinda look at everything, we look at the spectral analysis, we look at sides, what's different here, there and elsewhere, look at the EEG at the same time and then we do the evoked potentials. And the evoked potentials really are what show us what's going on because with the evoked potentials we're looking now in this half-second period of time, zero to 500 milliseconds, basically the brain's down and we're moving right on up through to the frontal lobe. So we know from other research, depth electrode studies, magnetoencephalogram studies where every bit of this is being generated within the brain. So we can deepen the brain from brainstem to cortex without putting depth electrodes in there or getting a $3 million magnetoencephalogram but you can't roll around all over the place anyway because it's a combination of MRI and EEG. But basically, and I'm coming back over there, what we see, the red is normal, the black is one of our patients. This is less than two standard deviations of difference. Here, at a quarter of a second, everything goes as they would say in East Texas to hell in a handbasket. Basically, we're going positive instead of negative. If you turn it over the other way, it's still significantly more reactivity. It's delayed because it's already too much and it can't go as fast. And then it comes back down to baseline. This is indicative of amygdala hyperreactivity at rest, just like when you go to the doctor and they take out their little rubber hammer and they hit you on the elbows and the knees and you've got deep tendon reflexes. If you relax, you'll have a one plus, two plus, three plus. If you engage your frontal lobe, it's not gonna move. It's just gonna hit you hard and pretty soon you're wrestling on the floor. There's no relationship left at all.  So basically, too many things moving. Okay, so in essence, this is 500 milliseconds. This is normal, the red, the black is delayed, excessive, wrong direction. It's like Mario, wrong way, wrong way, all wrong. Nothing's right, all wrong. Go back to go. And so this would be treated with the anti-convulsant. That's specifically the best one to do this out of many anti-convulsants. And this is soon to be revealed. Okay, and so this would be episodic rage reaction. What we have here is, as opposed to it, about 400 to 450 milliseconds, till the end of the wave form, it goes to flat line because it's already in the frontal lobes and you just, you know, you've heard 300 clicks. You're not gonna pay any attention to it.  So they're still gonna happen. You're not putting controls on yet. First, four tenths of a second, you're not controlling, you're just reacting and then you start controlling. This patient at 400 milliseconds loses total control and it goes up to here. I call that the energizer bunny. If you fall it out for another half second, it will not get back down to here. They cannot damp that response. So they have inadequate damping capability and excessive reaction, emotional reactivity, not a good combination. So what you do is look at what are, you know, what are the functions here? How does it function? Now this is visual on a different patient. And this patient is gonna only have one of the two problems. Basically, this is, because it's visual, it's a flash. It goes, it hits everywhere about 50 to 75 milliseconds quicker because it's going down the optic track. So like late at night, when everybody's not out on I-10, you can roll. The visual versus the auditory, the auditory hits many more semaphases. It's sort of like being, you get caught with a red light and stop sign over on the access road. So it just takes longer to get there. It's more sensitive, this is more powerful. That's why we do both. So basically this curve, the green curve is normal. This is the patient. Massively excessive reactivity would be thought to occur here, but it occurs instead back here, about 50 to 75 milliseconds earlier. So it's still coming out of the amygdala hippocampus system. So you've got a massively overreactive with a massive response going the other direction. And then when it gets into the frontal lobe, it flattens out. So the frontal lobes are working to control that. The issue is, this individual would present not with chronic irritability or not as severe chronic irritability because they're able to hold it, but they're stressing that frontal lobe the whole time. So, but basically the waveforms are the same. It's flat line, flat line, after about 350 milliseconds. And so they've got control.  And what you do see is episodic, more like intermittent explosives or eventually something triggers this individual and they go off. Road rage, whatever it is, it triggers them. And once it does, then it's Katie boy the door. They don't know what they're doing. They're beating the hell out. They'd be kicking somebody's car in, everything else. But they don't know this because when you're in fight or flight, that whole thing is set up because at least development is mankind and everybody else developed who came from the jungle, so to speak. You had to be a work to any threat.  And that thing is you need to react to any threat immediately because if you smell the leopard, that's why those smell areas go straight to the megalod. You need to run. If you're running the wrong way, turn around the leopards that way. Don't be looking around. There is the leopard because by then he's got you.  And so you can't go, oh, I give up. So you don't feel pain.  And this is how they are at that point. That's all they're focused on is, and the more sure before she do, the worse it gets.  They hear the noise, they hear the banging, they hear all this. They really don't know exactly what's going on, but it's not good. And at some point, they'll hear somebody close enough and they'll attack them. This is basically a P300. This time they've got earphones on, but they're going click, click, clack. It's a cognitive about potential. Their job is to, when they hear the odd ball, punch a button. And essentially what happens is in that normally, that will produce a third positive wave at 300 milliseconds coming out of the hippocampus directly. As shown, I can't point this thing down. There's no way I can point this thing down without everything going south. I guess that's because I'm pouring it down, right? That's concrete then, I understand. But you're also talking to yourself. I understand that too. But I'm having an excellent conversation. So what the hell? Okay, so basically this would be a normal P300 instead of, see this is the positive one, positive two, normally in an individual, but this is with a cognitive of both versus the other. This is that, but now with the cognitive of both, would the other thing even get a third wave, which will be abnormal without being in that circumstance, but we're evoking that by requiring them to cognitively attend to different frequent or infrequent oddball sounds. So this is, you know, it's like 60 or so microvolts. You only need five microvolts to pass the test. So this guy is obviously way up on the SAT. So this again, this is normal at 300 milliseconds. You get the start of this massive positive wave, electrically positive wave. This is P2, P2, P1, P2 and nobody home. There's zero microvolts. This is 67 microvolts. So basically if you put this patient on a stimulant and repeat this study, if you got the dosage right, it will go from this to this. As soon as the stimulant washes out, it goes right back down to that. It's not curative, but that's why they get a better retention on stimulant. Problem is stimulants overflow into the amygdala because it's so closely connected. So it cranks up the amygdala even further.  So, anti-convulsants for limbic dysmodulation, amantadine hydrochloride, or the other choice is either clonadine or guanphosine, which are alpha adrenergic agonists. Okay, we're getting there. All right, we're gonna be close. So, psychosocial, psychoeducational, they can benefit from that once you get them on the right medication. Carbamazepine, oxcarbazepine. We use oxcarbazepine. Brand name is trileptone. But basically, and carbamazepine is the second best, or essentially equivalent, it's tegratone. Those are the two. These are the dosages, or blood level by weight. Blood level or actual dosage by weight to titrate milligrams per kilogram per day, or 25 to 35 micrograms per milliliter blood level to get 85, 90% elimination of the explosive. And the abnormal P300, we use stimulus in the literature based 0.2 to 0.3 for dextroentatamine and 0.4 to 0.6 milligrams per kilogram per dose. Three times a day, because if you put them on the long acting, and you haven't got the other where it needs to be, they're gonna be raging 24 hours. We live with them, folks. We don't want that. We know what's gonna happen. If you get to these levels, if you get to the level that we're talking about, then you can put it in there and they work, and they don't blow up. Frontal lobe dysfunction, guanfusine or clonidine, both of which decrease norepinephrine or adrenaline flow to the frontal lobes because there's not enough break, so it's sort of like putting a brick under the accelerator when you really need to fix the break. And amantidine hydrochloride, which works by increasing dopamine activity at the D4 receptor specifically with minimal impact on the other receptors. There's six other receptors. And at the same time, it's an excellent agonist for dopamine D4, and it's a moderate antagonist for an NMBA glutamate, glutamate is stimulatory, frontally, but for whatever, most of this comes out of the head injury literature with the frontal lobe head injury.  So you get a glutamate cascade, so you're doing continual damage beyond the first original damage, so that's why they put the amantidine in, is to stop the glutamate cascade. So basically, it's stimulatory. It went up when the dopamine went down.  The brain is not always smart. It's big and it's complex, but it's not really that smart sometimes. But anyway, it should have gone down. So the dosage is for the amantidine, it's 50 to 200 milligrams per dose twice a day, six to eight hours a part. Doesn't last that long, give it first. Just like you and I need coffee in the morning before we attempt our ADLs and everybody comes in. What are we gonna do? You need to get to the car, you need to. Just let me awaken people, okay. These kids wake up with scrambled brains. And so the first thing you do is many times, the parents will wake them up for 30, 45 minutes ahead of time, give them the amantidine and then let them go back to sleep and then wake them up 45 minutes later and you've got a whole different animal. It works that quickly. And then you can give the other medications and they can do their ADLs and they can brush their teeth and not ripping their clothing and get no sock on one foot chew on the other one and wandering out the door. So basically that's it for medication. This again is the angry kid. This is the explosive kid. And like I said, all the contact information is in there. You can contact me at any time and I'll be happy to talk with you about whatever. When you get one of these kids, you see the rays stop the verbal de-escalation. They don't know who you are anymore. You may be their mother, their father, their therapist for the last eight years. They have no idea who this is. So whatever it is, it's a threat and they're gonna attack it if it gets any closer. No talk, remove the others, allow the rage if it's safe to occur. It will de-kindle faster that way. Rage face slowly, very slowly back away. If they follow you, threaten, curse, throw things, whatever, just keep moving back. You're not gonna take them down by yourself even though it's a five or six year old. You're not gonna do it. Not without getting hurt and them getting hurt. Remain non-threatening. That's not very usually difficult. If you dealt with many of these kids, you're scared spitless. You're not a threat, you just wanna run, Michael. Don't approach or touch unless you do not hold unless you have to for their safety, in which case you're probably gonna be holding for an hour until they're totally exhausted.  It's all about survival now. So we don't look. So when you, there's a thing, and I know it's somewhat controversial, but they're really not traumatized when you hold them because they're not there. When you debrief them and tell them what happened to them, that might be traumatic, but not when it's happening because I mean, they're just trying to survive. They don't know how they got there, what happened, whatever, and they're exhausted and usually wanna go to sleep. So, it's a different person than the person who has been traumatized and held and abused and so forth, but was aware of what was going on. That's not the case with these kids. They don't have a memory of it.  They're like, we're gonna get punished, what do I do? You did this, this, this, I'm sorry. That doesn't work, it doesn't change it. It punishes them for something that they had no control over. Again, just to reiterate, do not try to deescalate by right reason with an individual who is becoming irrational.  Of course that's never happened to me, but. Sheep. You don't try to say, no, wait a minute, darling, let's clarify this. You don't really wanna do that.  Really, that's ridiculous. You don't wanna do that. Try me.  Get everybody out of there you can. It will subside faster if there's less stimulation.  Sticks and stones will. And they don't get a weapon unless they just happen to stumble across one. The bad guys have got one hidden here and hidden there and once it starts, then they're gonna get you from behind while you're taking care of somebody else. These kids, unless they stumble over a chair and then they'll pick it up and hit you with it. But they don't even see it. That's why they stumbled over it. Just realize they're not there. Okay, summary, it's a new diagnosis. You have all this information, let's do Q and A. Can the moderators out there with the microphones circulate through the area? Actually, thank you, Dr. Matthews. Actually, if you have any question, if you can please come to the microphone here. It doesn't hurt because you're just not as narcissistic as I am, that's what it is. I have an attention deficit disorder. I can't get enough attention, but it's... I get enough dosages that it helps me. On the other hand, my narcissism is essentially invulnerable. So if you all walked out of here, I would not be devastated. You've got something else to do. Don't feel badly about it, okay? After all, I am a doctor. Good morning. Yes, ma'am. I'm wondering, since we know that the frontal lobe is very malleable, very plastic, and that it adjusts throughout childhood up through to the end of adolescence, why don't psychosocial interventions work just as well or better than medication? Basically, it depends on the degree, quite honestly.  These are so severe that unless you start to track differently, in other words, if you now give them, essentially, as I said, what happens is you have an epigenetic change, either with psychosocial, I'm not saying they don't, but it's basically they have to first be able to benefit from the psychosocial and they can't. I mean, they can't process that well. They can't deal with emotions without exploding. Just think of your borderline at the same thing. The same areas are dysfunctional in the borderline personality disorder and respond to the same medication. The hyperirritability, the explosive emotionality, the mistrust, they have some changes in terms of other brain areas, in terms of body image, et cetera, the right parol is one of those because that's how you project your own self image out into the environment and see it back. And the insula is right next to that and the insula is the housing of disgust.   Don't eat that. It's defensive, but the self disgust is kind of hooked into that parol dysfunction. So that's a whole different animal, so to speak. But it can't be borderline in childhood or adolescence. Anyway, you've got to turn 18 and then it's sort of like it's an error or something. Big, big coming out party. Now you are officially a borderline. Thank you, thank you, thank you, everybody. You know, you've just been something else before that. But if you put the medication in and then you are stimulating those receptors specifically, then that creates a demand for more receptors. And then you get a change, at least theoretically, may make a change. So it makes it faster. And then you can add the psychosocial in, which makes it even faster. So they're complementary, they're not one or the other. It's just sort of the rank order of what you need to do one and two. And it's like with the amantledine, you can get them where they need to be in five days. You just run it right up. We know right where it needs to go. It has virtually no side effects, no drug-drug interaction with all the other medications. We avoid any contoured events by knowing what works for what. And then we're still doing psychosocial, we're doing cognitive behavioral therapy, we're doing anger management, we're doing the other things. But we don't challenge them with that until they can feel success. Everybody's tried those and they can work, but we have to make it workable for this patient. Sort of like doing verbal psychotherapy, which is our strength, whoops, as opposed to with somebody who has no verbal memory after 30 minutes. Next time they come in, they can't. What did we talk about last time? Where were we? I don't know. Now you're being resistant, you know. You got it in there somewhere? No. I don't know. And some of it can be filing, that's why we do neuropsych testing on everybody. Is it because they can't file or they can't retrieve it after they file it? If so, we could give them one thing or the other. Okay? So excellent question, but they work in concert. Saved you a lot of frustration, okay? I know you do that well, but you gotta have somebody that can play nice in the sandbox. Yes, sir? So I think I have a similar question. It's about for clinical folks who are seeing a lot of kids, if we think about a continuum and kids who are outliers compared to the normal population and then kids that are sort of normal, what are some ways to differentiate when kids who are maybe on the boundary of what you're talking about and do you treat them differently? I mean, how do you know if you're dealing with, these kids you're talking about and what do you do with kids that are kind of on the boundary of that? Yeah, basically, you probably are best off, if anyone's considering putting them on an antipsychotic to get better control, you're better off going this direction. There is a research in molecular psychiatry that these guys were brilliant and they had the idea that they had identified 65, 67 different genes that were active in the brain and they knew what areas in which they were active in terms of their expression. So they took rats and gave them the equivalent dosage milligram per kilogram of cotyping that would have been given to a paranoid schizophrenic adult. And then they looked at the changes in gene expression because they know where each one of these genes is expressed and what they were looking at is if the cotyping changes expression up or down and we can tie down that this change is happening in this area because we already know that, then we can target our treatment better. Fantastic, a very sophisticated study. Problem is it proved to know how powerful it is because 34 of the 67, in every one of them it changed the expression, all 67 genes went somewhere. 34 would decrease the expression, 33 it increased the expression. So it was just random. So they couldn't figure out what to target, what was changing anything or if it was even changing the symptoms they weren't worried about it. The rats were not schizophrenic, it was just, you change that and there's arguments of rats are not the same as people. Some people would argue yes, some people would argue no, but bottom line is they are a good example. So it's like out of all of those and exposing them to cotyping, all they did was change the expression in every one of them and that's adult rats, that's not developing brains, that's my concern. If you're gonna do developing brains and you start changing, it's supposed to go up and you suppress it, that's not good or if it's supposed to be suppressed while you're doing something else and it goes up, that's not good. But we don't know because there's not been any research in that in terms of what it really does in the developing brain, which would not be, you couldn't directly do that anyway, I mean that would be unethical, but it's a question, a real question. Who else, anyone else? That's a good question, where is the borderline so to speak? But if you're thinking of medication for chronic irritability, et cetera, it's probably, if it hasn't fully blossomed, maybe sometimes it doesn't fully blossom until pubescence, as we know, both estrogen and testosterone totally blow the brain up at this point and it's making numerous changes and so all the wires are loose so it's sort of like, if you're having your house totally rewired and you come in and it's already late, best not to throw the switch anywhere until you've checked with the electrician, is it safe? Because hopefully he's shut down all the other connections, but maybe not. So basically, they've got a lot of loose wires up there and they've got changes happening in expression, all kinds of things going on, and as a result of that, that may be the point of which that's the straw that breaks the camel's back. They were kind of irritable and so forth before, but all of a sudden they became more explosive and one of the first things that I ask people when they call is, are they pre-pubescent? Well, yeah, they've grown some hair and they've done this, but I said, there you go, there you go. As now we really need to look. So, yes. Yeah, what role, if any, do you see psychological testing having in the diagnosis of this and also in understanding that kind of continuum that was just kind of... I think basically psychological testing is helpful in terms of designing therapies. Basically what we do is neuro-psychological testing that we're worried about neuro-cognitive deficits that frequently accompany these problems. Some of which you can pick up with the standard intellectual testing, the other great testing, the vendor, et cetera. But if it's more complicated than a full battery of neuro-psychology, it helps us and our patients are complicated. Trust me on that one. But when you're in the fringe, then you need to know, okay, for instance, if we're gonna do verbal psychotherapy, how do we reinforce that if they actually don't have very good verbal memory? Now, once you get them stabilized on the medication, it will progressively get better, but they also haven't exercised it. So they need to know, okay, well, how do I store this? And of course, first you need to be able to, we tell our people all the time, if you're talking to them, give them directions one step at a time and then have them repeat it to you and come back. That's retarded. No, it's not retarded. It's sort of like over and over the family will say, okay, now that you're on your medicine and all that, I want you to now start taking responsibility. I want you to take your plate, take it into the kitchen, scrape it off or right, run it down the dishwasher, run it down to the disposal and then I want you to put it in the dishwasher and close the door. And you go in and the plate is in there on the kitchen counter, nothing else has been done and they're back. What, what, what have I done? Yeah, you don't do three, four steps. You walk them through it, ask them if they got it and then you got it made. But even if they don't have the capability, even that's not gonna compensate for it, really. I mean, with any consistency. So psychological testing will help you on other things, sort of self-image and that kind of thing until we know it's damaged. I mean, if these kids frequently went on the unit and we get them stabilizing, they're doing much better. Of course, in the meantime, they're sort of surrounded by chaos, everybody's at a different level. But then they start looking depressed and somebody said, well, I think you need to put them on anti-depressants. Number one, don't, because that stimulates the limbic system and they're probably already on stimulants if they're really well stabilized. But number two, if you just now woke up and looked around and you could see everybody kind of like this when they're around you. Nobody wants to be around you. There's this huge space that you can't cross because everybody's protecting themselves.  And what am I gonna do about it? I don't have any skills, but now I know that whatever I did, I messed up all my relationships, my parents, my siblings, everybody else were terrified of me because they never know when they're gonna go off, he or she. And so basically you start with, this is how it works, and you don't, once they start getting success, nothing succeeds like success, like I said. That's the direction we want to be going. Not, you know, school punishes. That'll take care of it, dot, you know, never. I mean, they can't. When I was in school and I went to the principal's office, I corrected my behavior because I could. At least I would sneak you, I'm not sure how I would pan out on this test either, but one way or the other, you know, I got it done, I'm sorry, maya culpa, et cetera, et cetera. I won't do it again, at least not where anybody can see me. And for these kids, it's just not within their capability. Anybody else? Okay, I'll be around for a while if you wanna talk. And in the meantime, I know you've seen the schedule of this meeting, you're gonna be moving along. Okay, enjoy it, thank you, thank you. If everyone will please remain seated for a second, I have two very important announcements that affect your breakout sessions. So you're gonna wanna stay and hear this part. First of all, Dr. Matthews, what an amazing presentation. The bonus was how entertaining you are. I had no idea the humor that was about to hit this stage, so I think you can do a comic routine as well. So. Senior VP's at corporate. I was told by one of the senior VP's at corporate when I was having a lengthy conversation about the numerous failures of some of the people running some of the hospitals, but couched it in the same kind of term. She said, general, you ought to do stand-up comedy. I said, I got enough to do, and that's black comedy because these people are not doing right. You know.  So thank you. Okay, important announcements and important announcements. So first of all, last chance to go see your exhibitors. We'd like to thank the people right over here. Now cast SA, your public television on the internet for live streaming yesterday and today. It'll also be available on their website. As we mentioned yesterday, we've had many amazing sponsors and they are attendees here that are benefiting from those sponsorships because they're here on scholarship. So we'd like to really thank all the sponsors that really made this summit possible. We're gonna be finished after today's breakout sessions or breakout sessions, so I'd like to thank all of you for joining us. But very importantly, I have a whole cadre of people that volunteered either today, yesterday, or both days. If you volunteered and gave your time, please raise your hand. I'd like these people to be thanked for giving of their time. Now the next group of people I need to thank are the people that I get the chance to work with every day. They inspire me. They work so hard to help heal young minds and hearts so that our direct care providers can do just that.  Please raise your hand. This is an amazing group of people. Thank you and Gerard over here.  You'll get your certificate. You'll go to the next one. Now here's the two important announcements that you need to hear right now. The first is Mike Miller who spoke yesterday became ill so he is not able to be here today. So he's one of your breakout sessions today. I can see the faces like, oh, I was going to that. So here's what we're gonna do. We have free CEUs on our campus all the time. So what you wanna do is go to claritycgc.org. We're gonna have an obnoxious pop-up that asks for your email address. You can thank us for that. That obnoxious pop-up that asks for your email address will sign you up for our Clarity eNews letter so you will find out when we're having a free CEU on our campus where we're offering an ethics type presentation. So you're gonna wanna do that. So Mike Miller's session is canceled today but he was here yesterday and completed that one. Because we've had that cancellation, we have moved Dr. Gatanko to a larger room. So there's now more availability to go see her presentation. She's now in the Magnolia room. So Mike Miller's canceled. Dr. Gatanko moved to Magnolia. Have a great, great ClarityCon breakout session and thank you all.


Can you name some of the memorable teachers that you've had in your lifetime? Take a moment to think about your favorite teachers over the years. What made them so great? So effective. How about some of your least favorite teachers? No need to shout out their names, but was there a reason that they weren't as effective as the others? When you're giving an informative speech, your job will be to teach. Your goal should be to be the most effective teacher possible. In this video, we'll talk about who's giving speeches to inform, list some common general informative speech topics, and cover some of the familiar organizational patterns used in informative speeches. Let's get started. We encounter informative speeches each and every day. In fact, you yourself have probably given something similar to an informative speech sometime this week, if not today. For example, when teachers teach, they're informing. When bosses give sales updates and explain policy changes, they're informing. When coaches coach, they're informing. When pastors and other clergy give sermons, they're often informing. When parents or friends share information with us with the goal of imparting knowledge, yep, you guessed it, they're informing. In your everyday interactions, you often need to be able to both give and receive informative messages. Because of that, you'll want to know how you can be the most effective. Before we get to that, though, what are all these informative messages about? Informative speeches can be about pretty much anything, but some common topical areas include speeches about people, places, objects, tacos, actions, processes, events, plants and animals, phenomena, issues, ideas, cats, concepts and theories. If you need some advice on selecting a speech topic, we have a video dealing with precisely that process that can be found on the Compadres Media YouTube channel. To make sense of the topic and help the audience understand and retain as much of your speech as possible, it's important to organize it properly. You've probably already learned about organizational patterns. If not, once again, we have a video on that very topic on the Compadres Media channel. But it bears repeating, as some of those patterns are a better fit for informative speeches than others. For example, process or historical speeches will likely use a chronological pattern. Speeches about places or events might use the spatial organization pattern, which follows a directional flow. A comparative pattern might be used when moving from the known to the unknown or for objectively presenting information about options. The same objectivity would be a hallmark for an informative speech using the pro-con organizational pattern. Pick a topic and then present an unbiased view from both or all sides. The causal or cause-and-effect pattern is great for explaining both what is happening and why. The topical organizational pattern, which simply selects and places main points in a logical order, would work for almost any informative speech topic you can think of. The key to picking the correct organizational pattern is determining which will be the most effective for the information that you plan to present. Start with the end in mind, having a firm understanding of the goals of your speech and then consider which method of organization will best accomplish those goals. So what kind of teacher are you going to be? Carefully considering and selecting the topic for your informative speech and matching it effectively with an appropriate organizational pattern could make all the difference in determining which list you end up on for the folks in your audience. Choose wisely.