Welcome to our seminar. It's really a pleasure to see you all and see that we have such a lovely audience. We look forward to presenting and also some discussion about these interesting topics. We are Drs. Venigala, Shibuk, Van Nostrand, and Dr. Safar from Leahy Hospital and Medical Center in Massachusetts, and we are going to present on these very interesting and some of them controversial topics at the intersection between neuropsychiatry and consultation with some psychiatry. So we hope you enjoy the agenda for today. We are going to start with a discussion of the differential diagnosis of delirium and the intersection with acute psychosis. We are then going to continue with a discussion of the diagnosis, the presentation, the treatment of the syndrome of catatonia from the perspective of when you see catatonia in the inpatient medical setting, specifically. And then we're going to talk about the controversial syndrome of delirious mania, which has a little bit of a combination of mania, delirium, and catatonia. We have no relevant financial disclosures to make, and this is the agenda for today. We are going to allow a couple of organizational things. We're going to allow for one or two questions in between talks, and then we're going to have longer time at the end of the three presenters for Q&A. This session is being broadcasted online in addition to you all attending in person, so we are also going to be receiving questions from the online audience. In that case, I am going to read the questions so that you all know what we are talking about, okay? In terms of our speakers, Dr. David Van Norstrand is the director of CL Psychiatry at our hospital, Leahy Hospital and Medical Center. He obtained his medical degree from Mayo Medical School, where he also completed a Ph.D. in molecular pharmacology and experimental therapeutics. He completed his psychiatry residency at the combined program between Mass General Hospital and McLean in Boston, Massachusetts, and a fellowship in CL Psychiatry at Cambridge Health Alliance. In our hospital, he's also the director of the clerkship for medical students, and he is an assistant professor of psychiatry for Tufts University Medical School. Dr. Larry Shebook obtained his medical degree from BU, Boston University Medical School. He completed his psychiatry residency at McGill Hospital in Montreal, and his very interesting psychiatry career in clinical and research aspects spans different institutions, both in Canada and the U.S. Before joining Leahy, he was the medical director of inpatient psychiatry at Marlborough Hospital, which is part of UMass Chan Medical School, and now he's attending psychiatry both in our CL and our outpatient services in Burlington. And Dr. Hema Venigala completed her medical degree at Dr. PSI Medical College in Chenotpally, India. She completed her psychiatry residency at the Wright Center in Pennsylvania. She has coauthored several articles, both in clinical psychiatry and biological psychiatry, and has presented numerous papers and abstracts at the APA as well as the biological psychiatry meeting. And he's an attending psychiatrist also at the Leahy Hospital. So with that introduction, I am going to let you enjoy the talk from Dr. Van Olsen. Thank you for your attention. Thanks Dr. Safar for that kind introduction, and thanks all of you for being here this afternoon in, for now, sunny San Francisco, or joining us virtually from wherever you are. So first, I have the privilege of presenting a topic that's very near and dear to my heart as something that we encounter every day in CL psychiatry, this common question that comes up of, is it delirium, is it psychosis, and does it matter? First of all, we're going to look at sort of the relationship between psychosis and delirium, sort of looking at it as not so much an either or, but a both and. We'll better characterize the psychiatric presentation that may masquerade as delirium, which will hopefully give us a clear framework to approach cases with both psychotic and delirious elements. So just to kind of frame your thinking a little bit as we kind of go through this, and we'll come back to the answer at the end, which of the following presentations of psychotic symptoms would typically be expected to have an abnormal EEG? Catatonia, Ganser syndrome, delirium, manic episode. We'll come back to that at the end. So we'll start with a case, a case that we saw in our consul service to kind of frame this discussion for us. We'll then look at an overview of delirium and psychosis. We'll come back to the case, and here we go. So this is a 63-year-old female with a history of post-traumatic stress disorder and anxiety on chronic benzodiazepine treatment presenting from the proverbial outside hospital for convulsions, status post restrained motor vehicle collision. So on the day of admission, she's driving home to her sort of home in the Boston area from Cape Cod, and the stress of driving triggers a panic attack. Now, we had heard from her sister that she did actually receive a driving citation just prior to this presentation as well. But in this case, she actually drove onto someone else's lawn, bystanders called EMS. And when they got to her, they found her awake, but she wasn't really following commands. She wasn't really responding to EMS. And she was brought to the outside emergency department. During the course of the HMP with the ED attending, the patient actually developed leftward gaze and body twitching, which was then broken by lorazepam 2 milligrams IV. This episode then repeated itself after 30 minutes. And shortly thereafter, she had a generalized tonic-clonic seizure, which resulted in intubation, loading with 3 grams of levotiracetam, and then she was transferred to our hospital's neuro ICU for further care. She was extubated on day 1. And during the next week, she had these episodes of what were sort of termed in the nursing notes as confusion, speech arrest, with and without EEG correlate. And we were consulted on hospital day 8 due to what was noted to be intermittent paranoia. And this raised the question, is this all related to delirium? Should other diagnoses be considered? And what is the general approach to psychotic symptoms in a patient who appears confused? What does that even mean, confused? So we throw around these terms a lot. We talk about altered mental status. We talk about confusion. We talk about is the patient delirious? Do they have encephalopathy? Are they encephalopathic? So first a few notes on these terms. So first of all, altered mental status is sort of an umbrella term, rather imprecise, just sort of suggesting that the patient's mental status is different than it was before. Confusional state, we often talk about a patient being confused. Also a fairly imprecise, impaired level of consciousness, a more sort of severe clouding of sensorium than their typical thought process. We talk about delirium, which is in fact a diagnostic entity that we'll get to that does have diagnostic criteria. And then this fourth term that's often used, encephalopathy, which depending on which service you may be interfacing with, they may have a slightly different understanding of what that represents. Here we're sort of using it interchangeably with delirium. It's often used by neurology, for example, when they talk about toxic metabolic encephalopathy. And interestingly, in sort of DRG coding world, it's actually coded as a higher weight medical condition than delirium. Even though clinically it's interchangeable, our service typically bills for encephalopathy, which conveys a high degree of morbidity and mortality, which we'll get into. Focusing in on delirium, DSM defines it as a disturbed attention and awareness that develops over hours to days, is a change from baseline, and is fluctuant. We have to talk about it waxing and waning. Has a degree of additional cognitive disturbance, which we'll get into. And it has the clear caveat that it's not attributed, this attentional impairment with cognitive disturbance, it's not attributed to a reduced arousal or the developing or established neurocognitive disorder, like dementia. And then importantly, it does have evidence of a causative medical condition. Now in terms of additional cognitive disturbances pertinent to our discussion, this can include psychotic symptoms in addition to memory disturbance, language impairment, executive dysfunction. Patients can also have psychotic symptoms. Now we know that delirium itself carries a number of long-term consequences. We see higher mortality rates in delirium, higher rates of a future dementia diagnosis, longer lengths of stay, and importantly, as we often see on the consul service, an increased risk of harm for patients and for staff. Looking particularly at psychosis in delirium, it's been demonstrated in various cohort studies that at least 40%, if not more, of delirious patients have delusions and hallucinations, which themselves carry a high risk of psychomotor agitation and aggression, risks of self-harm inadvertently, often risks of harm to others, non-compliance with critical medical interventions. This is often where we're consulted, but that carries with it its own set of potential risk for bias. So for example, Ross et al., a number of years ago now, looked at consultations to psychiatry from delirium and found that psychosis in delirium tended to more likely lead to a psychiatric consultation. And so that suggests, or at least begs the question, are we at risk then of being biased towards psychiatric diagnoses when we encounter these situations? And the risk kind of comes in two directions when we're encountering psychosis and thinking through its differential. We risk missing delirium, and we risk missing a primary psychiatric illness, which each have their own potential for negative sequelae. So for example, in missing delirium, one risks medical deterioration and the aforementioned negative outcomes that we associate with delirium. We risk an inappropriate psychiatric admission. The patient may be quote-unquote medically cleared and then transferred to a hospital that is not the ideal place to treat the delirium and the related underlying potential medical causes. And then we may see the iatrogenic medication administration, whether benzodiazepines, which we know can perpetuate delirium, or antipsychotics, which are attempting to treat psychotic symptoms which have a medical cause. On the other side of things, we risk in attributing it just to delirium, we risk missing a primary psychiatric illness and thereby delaying psychiatric treatment, whether related to medications or workup in terms of family and patient history. We risk inappropriate medications on the other side, for example, treating with antipsychotics for what ends up being potentially a medical or maybe a psychiatric cause of catatonia, which we'll talk about a little bit later. And then we may not obtain the history that is appropriate to ascertain the presence of something like Ganser syndrome, which we'll get into a little bit later as well. So as we're encountering this situation and we see delirium on the differential diagnosis, what should we be considering from a psychiatric perspective? And I would offer a number of these and would commend to you this review from Wilson et al., which really goes through a lot of these pseudo delirium psychiatric presentations. So we have delirious mania, which Dr. Venugala will talk about, psychiatrically induced catatonia, which Dr. Shabook will talk about. We have potentially disorganized psychotic presentation, Ganser syndrome, and then I would add Lewy body dementia, which often has a challenging workup to distinguish it from delirium. We'll go through each one of these briefly. In terms of delirious mania, and again one slide on this because we have another presentation on this, but as we know it comes with it a historical context and somewhat of a controversial nomenclature, which we'll get into. And it's often difficult to distinguish from delirium in the variable clinical status of symptoms, as well as occasionally autonomic dysfunction itself. And we may see an extreme motor dysfunction lab abnormalities, such as elevations in creatine kinase, leukocytosis, potentially signs of renal failure. It's important in that context to look for, is there evidence of a bipolar diathesis? What was the history leading up to the presentation? Do they have a known history of bipolar disorder, medication not adherence, signs of psychiatric decompensation prior to admission? Is there evidence of catatonia, which can often sort of overlap as we'll talk about. And importantly, there's often here, as we'll talk about, a role for benzodiazepines that is typically absent in delirium, and that's where the distinguishing features can be helpful in informing the course of treatment that one would chart. In catatonia, which we'll talk about, the EEG, which we were able to get in this lady, and we'll talk about what it showed, is typically normal in mania, normal in psychiatric causes of catatonia, versus the diffuse slowing that we see in delirium, even though the patient may in fact be stuporous at the time that we're seeing them and seeing that they look similarly to a delirium. The Bush-Francis scale may be helpful in distinguishing features in the response to lorazepam challenge, which we'll talk about in depth, is often thought to be diagnostic, although it can be challenging in a medically compromised patient where one might not be as aggressive in the dose of the lorazepam as we otherwise typically would be. And the last note which I've mentioned before is the caveat that the causes of catatonia can often be medical, and then you have sort of a syndrome overlap with delirium, which can present its own challenges in terms of treatment. In terms of disorganized psychosis, so a patient presents with schizophrenia, a substance-induced psychosis, there's typically no notable EEG correlate. They're going to be typically more clinically stable than they would in delirium. They tend to be more often alert, less so typically over time in delirium. The language tends to be more disorganized in disorganized psychosis as opposed to in delirium, although you may see paraphasic errors, for example. And importantly, non-auditory hallucinations are fairly uncommon in disorganized schizophrenia. Visual hallucinations tend to be more generally vague, shadowy, may have some mood congruent quality to them as opposed to bugs crawling on the ceiling, a family member sitting in the room, that sort of thing, which is more typical in delirium. Ganser syndrome, which is first of all rare. It was identified first in or mentioned in 1897 by Dr. Sigbert Ganser in Germany in a prison population of patients awaiting trial. And the idea is that it's an unconscious psychological escape for an intolerable psychosocial situation. A central differentiator on the physical exam is going to be the patient providing approximate answers to questions. How many legs are on a dog? Five. How many hands are on a clock? Three. Sort of approximate but erroneous answers to questions. The EEG is going to be normal in this case. And the psychosocial history is going to be key here. There's going to be a recent trauma, there's going to be legal charges, some other very acute traumatic stressor present in the patient's recent history. And the approach here is going to be similar to that of conversion disorder, where typically psychoeducation reassurance to the patient around this presentation is a central key feature of the approach. But it's also important to consider factitious disorder and malingering, which are both conscious efforts to obtain either primary or secondary gain. And naturally that can often be hard to tease out. And then lastly, Lewy body dementia. We talk about it in its probable diagnosis definition because Lewy body dementia is definitively diagnosed at autopsy. But probable dementia with Lewy bodies is a clinical diagnosis with progressive cognitive decline and then two out of the following three, fluctuating cognition, which I've underlined as being very similar and overlapping with delirium, recurrent visual hallucinations and spontaneous motor Parkinsonism. Highlights the challenges of distinguishing delirium from dementia and that you do have a lot of symptom overlap but there are ways to sort of tease out and distinguish the two. Unfortunately, EEG is typically not one of them as findings are similarly very similar with generalized slowing. Motor disturbances are present in 25 to 50% of cases and are typically gonna be Parkinsonian as opposed to typically in delirium where it's gonna be more psychomotor agitation or general retardation. The presentation is typically gonna be more insidious and this is where you're gonna rely more on family history, sort of pre-hospital history and there is gonna be importantly more antipsychotic sensitivity and that might help you refine your diagnosis if the thinking initially is delirium and then in treating with antipsychotic, there are Parkinsonian symptoms that get worse. And then interestingly, postural instability tends to be more of a feature of Lewy body dementia whereas in delirium, the patients are often weak or deconditioned but there's not as much of that clear postural instability as you'll see with Lewy body dementia. Circling back to the case. So the initial EEG that we saw in this particular woman showed frequent prolonged focal seizures. So she was in fact having seizures in her presentation. The EEG on the day of psychiatric consultation which was helpful to us did demonstrate occasional admixed delta-theta slowing consistent with a fluctuating mild to moderate generalized encephalopathy. She was noted on our exam to be anxious. She noted panic attacks over 10 years and the only thing that was helpful was clonazepam one milligram four times a day. We weren't entirely sure if she had been entirely compliant sort of taking that consistently leading up to it and so there was some thought that some of the initial seizure may have been in fact withdrawal and it was provoked in that way. She had no history of trauma although it was notable that when a man entered the room, she appeared hypervigilant and then sort of just said quite loudly, there's a man in my room. Over the next week, she had a fluctuating disorientation. Nursing notes were very helpful in this regard. Forgetfulness, at one point she accused staff of trying to kill her. She was combative requiring IV haloperidol and she had episodes of aphasia. We said this is delirium and should be managed as such. We were reconsulted on hospital day 15 and saw that she had been having slowed speech. She was still tangential and the evaluation psychiatrically noted that she had difficulty maintaining attention, often loses track of what she's saying. She's restless and fidgety with the EEG wires. The patient endorses feeling confused and that some days she is clearer than others. She had attended this presentation earlier. She is forgetful and at times seems to be oriented to being in the home and other times she thinks she's in the hospital and she also references thugs who were threatening to her. And so what we said is, this paranoia is in the presence of disorientation, clouded sensorium, she's slowed in her reaction, her answers to us. She has impaired attention. We felt like this was delirium and not a primary psychosis and encouraged the ongoing medical treatment. She remained unfortunately impulsive intermittently and confused, agitation at night which include paranoid themes. The sitter kept having to redirect the patient to the room and she would tell us she felt safe but then was telling nursing that she felt unsafe. And see where I'm going with this. Agitated behaviors from paranoia were preventing rehab placement. So we got the understandable often, the common request from case management, can she go to Jerry Psych, please? What we said in our response to that understandable question was, there's no evidence of mood disorder. The anxiety appears baseline here. And so it's hard for us to attribute her impulsivity to an underlying psychiatric history. She has a history of depression and anxiety, does not seem to be that she has an increased amount of depression or anxiety at this time. She has impaired concentration with paranoia and intermittent agitation. So kind of a waxing and waning of her agitation. Her EEG shows diffuse slowing which would be absent in a psychotic disorder. We believe that this is delirium or encephalopathy and not a primary psychiatric condition. And therefore the disposition for us, our recommendation is rehab, not a psychiatric unit. Because as we know, one of the most effective interventions for delirium is early physical mobility and rehabilitation. And so we argued for what we felt would be the more helpful disposition for the patient. We did add some Depakote targeting her impulsivity which was a sort of a temporizing measure in our minds to kind of help her get to rehab. But we did not recommend that that be continued indefinitely. So in conclusion, we've talked about, we've seen, we've experienced that psychotic symptoms are common in delirium. And we know that multiple psychiatric presentations can mimic elements of delirium. We're gonna talk about two of those in just a moment. But that the treatments themselves are not entirely overlapping. And so it's more than just academic that we're able to distinguish between these various phenomena. Premature closure then in either direction risks exposing the patient to unnecessary treatment and or delays in care. And the elements of the history and the mental status exam and at times the physical exam can help distinguish delirium from its psychiatric counterparts. So coming back to this, and if you're brave, you can raise your hand. Which of the following presentations of psychotic symptoms would typically be expected to have an abnormal EEG? Would we see that in catatonia, in Ganser syndrome, in delirium, yay, or in a manic episode? No, okay. So in fact delirium. So some references and these are on the app. And then I did reference in my talk two reviews that I commend to you. First by Dr. Wilson et al and then Oldham et al around that interface between delirium and other psychotic entities. Thank you. Thank you, David, for a great presentation. As I said, I'm going to allow for one or two questions now if anyone wants to ask them, but we're going to have more time at the end. Go ahead. I had two thoughts. One was this woman was on huge doses of, can you hear me? Huge doses of benzos. So I was wondering about whether there was any evidence of a dementia kind of syndrome. She was in her 60s. The other question is if she was paranoid enough during the evenings to consider using tiny doses of Risperdal or something like it for that aspect of her illness, if it was causing enough discord on the unit, shall we say? Yeah. So just to repeat the question, one was that she was on a very high dose of benzos and we know that chronic benzodiazepines use can predispose one to dementia. So was there an early dementia developing here? And then secondly, what was our approach in terms of, given that her psychotic presentation seemed to be somewhat disruptive on the unit, did we start an antipsychotic? To the first question, I think it's a great question. As you know, it's often challenging to distinguish between the early sort of signs of dementia and some of the cognitive dysfunction that we can see in delirium, except for to sort of repeat the exam serially. And she did, her cognitive status did improve significantly over the course of the hospitalization. So while one wonders if down the road, there are some harbingers here, but at the time we did not see dementia as sort of the leading edge. In terms of our treatment approach, the barrier to rehab, which was kind of what we and the team were focused on because we just wanted her out of the hospital to get to a place where she could start getting better, was the impulsivity. And so we just, we happened to choose the Depakote for that. I think, more than anything, she was presenting as odd. And I think that's what triggered the initial consult. Go ahead. And this is gonna be like a 30 seconds question, 30 seconds answer. It's a two second question. Any thought that the Keppra might have been perpetuating the psychosis? The Keppra question. We often get the Keppra question. It's a fair point. Keppra is often used by neurologists. You don't have to check the levels. It's a very sort of benign medication from their standpoint, but carries with it the sort of neuropsychiatric contributions. Hard to tease that out, but it did sort of come up if she was initially loaded with the Keppra. I think we thought it was most likely post-ictal, but there were potentially elements that that contributed to. Thank you very much. And we're going to now hear from Dr. Schiever. Dave told me before the talk that probably most of the people in the audience would be CL psychiatrists and I have a feeling he was right because when he said the word placement there was a huge roar from the crowd. Okay, so I'm going to talk about catatonia, and the message of this talk is actually pretty simple, and it parallels my own trajectory of what I learned about catatonia, when, and then how it affected what I did in the clinical world. How about now? Better, yeah. So the message of this talk is actually pretty simple. It parallels what I learned about catatonia, and how it affected what I do clinically, and actually the first two lines of this slide, catatonia is hidden in plain sight, and finding catatonia requires knowing what to look for, are actually really the takeaways for the talk, and I think this is specifically, possibly more true for me because of when I was trained, but I think when you were trained sort of influences how you thought about catatonia, what you, when you see a patient, what comes to your mind. So historically, going back to the 19th century, catatonia was originally defined by Kalbaum as a separate psychiatric illness, and then later by Kreplin as a particular type of, or a symptom of a particular type of psychiatric illness, catatonic schizophrenia particularly, but the concept that catatonia could be secondary to medical or neurologic disorders came much later, and that's, it's the evolution of that thinking that I'm gonna talk mostly about. So I remember when I was a resident studying the chapter on schizophrenia, these fantastic pictures of patients in these unbelievable postures, and I never saw one, or I might have seen one, but I didn't know it. So going back into the history, middle of the 19th century, called Kalbaum, he conceptualized catatonia as a separate psychiatric illness, and he described both forms of what we see clinically, the stuporous and retarded form and the excited form. I'm sure you're all familiar with those. Kreplin, as you probably know, was the first to provide a classification of psychotic illnesses, and he differentiated psychotic illnesses into what he called manic depressive insanity and dementia precox. Manic depressive insanity we now know as bipolar disorder, dementia precox we now know as schizophrenia. But along with, one of the interesting things about catatonia is that it kind of parallels a little bit about evolution of psychiatric diagnosis and what happened in American psychiatry and in the world. At the beginning, there was a strong medical emphasis in psychiatry, and then there was a period where that wasn't so prevalent, and then later there was another period where it returned, which is kind of where we are now. So in the first half of the 20th century, there was more of an awareness that catatonia could be caused by medical conditions. And one of the most quoted authors with respect to catatonia is someone named Fink, and his term for catatonia is a systemic medical syndrome. And he described it as extremely prevalent in post-encyphalitic states or other neurologic conditions. I wanna emphasize post-encyphalitic states because that'll come up on a slide later. But just another brief historical point about encephalitis. Some of you are probably familiar with Oliver Sack's book, and then there was a movie called Awakenings. And that was historically kind of important for neuropsychiatry and everybody else, but there was this epidemic in the early 1900s, encephalitis lethargica, or what was called post-von Economo's encephalitis. And Oliver Sack's, when he realized that many of these patients had, he found them basically asleep in nursing homes all over the place, and he gave them dopamine, and he realized many of them obviously had post-encyphalitic Parkinson's. But when he also went back and looked at the records of the patients from that epidemic, he found that a significant number of them actually had catatonia in a post-encephalitic state. So psychiatry is still part of medicine at the beginning of the 20th century, and then there were some early findings which sort of foreshadowed things that we now know to be true. Catatonic symptoms respond to sodium amytal. Sodium amytal is a sedative hypnotic. It does the same thing to the brain as benzodiazepine, so people knew about that a while ago. And then the modern era came with the introduction of psychoactive drugs, and then neuroleptics were introduced, and then the original description of what we now know as NMS was called a quote-unquote neurotoxic reaction. And that's important because pathophysiologically people think catatonia is somewhat on a spectrum of NMS. And then historically, people were always aware of something called lethal catatonia. Maybe it wasn't as well described as it is now, but people knew that it responded to ECT. And now we know that the definitive treatment for catatonia is ECT. So Freud arrived in America, and then catatonia fell asleep for a while, and then it woke up again. And I think what I'm trying to say is that there was a while in American psychiatry that was fairly dominated by psychoanalysis, and then there was kind of a turning point later when DSM-III came out where people brought psychiatry back into the mainstream of modern medicine. And this is actually kind of the beginning of the modern era. Two people I'm very fond of, their writing is Taylor and Abrams, and they did a lot of studies in the 70s on bipolar patients, and they found that catatonic symptoms were highly prevalent in bipolar patients, both mania and depressed phase. And in fact, it kind of turned the way we think about catatonia, at least from the psychiatric perspective, a little bit upside down, because now we know that about 70% of patients who have catatonic symptoms secondary to a psychiatric illness are bipolar and not schizophrenic. So when you see a patient and they're catatonic and you know they have a primary psychiatric illness. If you have this thing in your brain that says schizophrenia, you should switch it around to a mood disorder. Later on, there was an awareness that catatonia can be secondary to systemic medical conditions, infections, metabolic conditions, neurologic disorders, epilepsy. And then the modern way to describe catatonia, at least I think this is Fink's term, or many people use the term, is a psychomotor syndrome. So why is it important to recognize catatonia? I just want to leave out something that actually was sort of pretty important. So I had an occasion a while back to read a lot about catatonia and, you know, in the back of my mind was catatonic schizophrenia and I happened to be working on an inpatient unit and then all of a sudden it just kept popping out of the woodwork. So it was something that I hadn't been aware of and then once I had done all this reading about catatonia, it was actually really popping out of the woodwork all over the place. So why is it important to recognize it? Well, it could be lethal, that's number one, and then thinking a little bit like Dave went through the diagnostic process of delirium, we use a similar diagnostic process for catatonia because we have to identify, it's really the tip of the iceberg. We have to identify what the underlying cause is and the underlying causes could either be psychiatric or non-psychiatric. And the last point is that catatonia is extremely treatable. Okay, I'm going to present a couple of cases that we had on the consult service at our hospital. A lot of us know who they are. This was a 60-year-old woman who presented to our hospital, having been transferred actually from an outside hospital, and she had a one-month history of mild frontal headaches, non-radiating fatigue, inability to concentrate, and then showing major personality changes at home, seeming laughing inappropriately. The outside hospital got the CT scan, and then that's what the CT scan showed initially. The brain biopsy was performed, and she had primary CNS lymphoma. So she was transferred to our hospital for her definitive treatment, and then a couple of days after she arrived, we get called. She's completely psychotic. We do the usual thing. We start antipsychotics. A couple of days later, we're called. She's catatonic. We do the usual thing. We give her IV lorazepam. Her catatonia goes away. The neuroleptics are stopped, and someone brought up the Keppra. The Keppra was also stopped, and then once the neuroleptics were stopped, and she was transitioned from Keppra to Depakote, the delirium and the catatonia resolved. This is another case we had on the service, and he kind of almost became a member of the family to our service, because he came in every year for about four years. He's an 81-year-old retired male with a history of recurrent catatonic depressions, and every time he came in, we were called, and he came in completely unresponsive, and then he got IV lorazepam, and then he immediately woke up. So it was sort of no mystery. The difficult part was sort of managing him until he could get transferred to an outside hospital for definitive treatment. I thought, I was always wondering why he ended up at our hospital, because we always knew he had ECT. He responded to ECT in his past. His daughter was a physician, and then I spoke to his daughter. He said, well, why is he always coming here? Why do you always bring him here? And he said, well, the EMS protocol is that anybody who's unresponsive has to go to the nearest hospital, so he comes to our hospital, because he lives nearby. But he always had responded to ECT. He was reluctant to go for follow-up, and then on his last admission, his daughter told us, and the patient told us that he had formed a good relationship with a psychiatrist who treated him with ECT, and then he agreed to go for maintenance treatment. So, these are all the things that can cause catatonia. Okay. The column on the left are primary psychiatric illnesses. Middle column, neuromedical and substance-induced. And as I said before, I think the most consistent findings that I've read are of the psychiatric illnesses that can cause catatonia. Most are probably mood disorders. We actually had one, and some of you may have sort of seen this similarly. How do you sort of, what's the overlap between other psychiatric illnesses and dissociation? So, we had one where we were going back and forth. Was it psychosis? Was it dissociation? But just as an important point, dissociative disorders actually can lead to catatonia. In the middle column, I presented the case that had a primary CNS tumor, and then I don't think we have had any in the last column, the substance-induced. We had a case, and I think, I don't, I'm not sure I can actually sort of explain this, but people sort of seem to think that there was a patient who was abruptly stopped from high doses of clozapine that ended up catatonic. Okay. The, a lot of the remaining slides are taken from the American, the Academy of Consultation Liaison Psychiatry produced a how-to guideline, basically a clinician's guide to the diagnosis and management of catatonia, and a lot of the remaining slides are from that monograph. I thought this one was a useful one. It's just a mnemonic, slime posture. So, it was kind of interesting what, once I became more aware of what, you know, what catatonia can present as or look like, the rest of the people on the unit know, and then there's kind of an increasing sort of awareness, oh, that patient hasn't come out of his room for three days, he's not eating, he just stares into space, and then it's catatonia. So, things to look out for, speech, decreased amount of speech, and particularly increased latency of speech, and people who don't interact with other people. So, that could be a catatonic presentation, and then muscle tone, increased or decreased, and staring, I remember a patient who came in, to an inpatient unit, who was so manic, got the standard cocktail of lithium and Haldol for two days, and then two days later was sitting in a chair, absolutely mute, staring into space. She wasn't rigid, and she'd been on lithium and Haldol for two days, and gave her Ativan, and then she was going a mile a minute, and then when we stopped her Haldol and just gave her lithium Ativan, the manic episode resolved. Posturing, people sort of assuming weird postures. If anybody kind of looks like they're in a strange position or something like that, then you can think about catatonia. So, when you have two or more things that kind of increase your index of suspicion for it, and you kind of go into what's the more well-known detailed exam, and I'm not going to go through all of the symptoms, I'm sure you've kind of gone through them, but I just want to point out that there is a standard rating scale for measuring catatonic symptoms. It's called the Bush-Francis Catatonia Rating Scale, and it's kind of their, there's a website I can direct you to at the end, but basically you do a screening exam, and then if they come up with some symptoms, you do more symptoms, et cetera, et cetera. Okay. So, this is what the actual rating scale looks like, and you can print it out from their website. Some theories about the pathophysiology of catatonia. Motor system dysfunction. Well, obviously, motor system has to be involved because they either don't move or they're stiff or they're moving too much. But pathophysiologically, the same areas in the brain are thought to be involved in catatonia and NMS. We know neurotransmitters are involved. GABA certainly has to be involved because it responds to benzodiazepines. Dopamine is probably involved because antipsychotics can either precipitate catatonia or make it work, make it worse, sorry. Epilepsy, there's thought to be a higher prevalence of seizure disorders in patients with catatonia, and then endocrine metabolic, possibly because ECT is effective for catatonia, and ECT can normalize the hypothalamic pituitary axis. Okay, again, these are from the Academy Consultation Liaison Guidelines. So you've got to do the differential diagnosis and consider pretty much everything, and then they recommend looking at people into two groups, people who can't interact, which are the catatonics, and the people who won't interact. Those include malingering and factitious disorders. Another caveat here is that someone who's persistently delirious and not responding to treatment think that catatonia could be a possibility. Okay, basically, this is almost a repetition of a delirium workup, but you've got to sort of look at all the bases, metabolic, infectious, endocrine, substance abuse, CNS, epilepsy, cardiac conditions, and then now becoming, I'm not sure if it's more prevalent, but people are more aware of autoimmune encephalitis as causing catatonia, and people are looking more at that. And then when you get into the more severe spectrum and you start to see signs of NMS, and then you're looking, obviously, at higher levels of care, and then the patient is in the ICU. Okay, so fortunately, at least while I've been working at our hospital, we haven't had severe spectrums where we've had to transfer people to the ICU. So the treatment of catatonia, when you're just looking after them in the general hospital, isn't really that complicated, but it's actually pretty important because they're not eating, they're dehydrated, whatever. So it's basically simple supportive care, stopping neuroleptics and other dopamine depletors. And then when you start to see the autonomic instability, then you start to get worried, and then you have to start thinking about more severe conditions like NMS or malignant catatonia. Treatment, the IV lorazepam challenge, we do it in our hospital, usually IV, because the patients that we're seeing already have lines in, so it's much easier. On a psychiatry inpatient unit, I've given it, I am, and it works just as well. And then lastly, the patients who don't respond to conservative management, ECT. I put up this slide, Laura and I were looking around for slides. They would kind of give people an idea, well, what are the things in the hospital that cause catatonia? And we didn't find one for a general hospital setting, but we found this one, which was statistics from a tertiary care neurologic center. And there are a couple of things that I thought were interesting here. Under neurologic, I don't know if you remember back at the beginning when I was talking about Oliver Sacks and encephalitis, the largest number of patients who had a neurologic cause for catatonia in this hospital had encephalitis. I found it a little bit surprising, based upon at least my reading, is that in the psychiatric section, the cause, they found that schizophrenia was the highest disorder. Okay, so finally, catatonia goes way back. And the best way to think about it currently is that it's a psychomotor syndrome. It's important to recognize it because it can be lethal. It has, like delirium, a number of treatable causes, and it responds to treatment. And then, perhaps most importantly, you won't find it unless you kind of know what to look for. And these are some suggested readings. I'm not going to try and activate this link, but this is a link to a website that was produced by the psychiatry department at the University of Rochester. And I really recommend it because they basically get complete training, not only in how to do the Bush-Francis catatonia scale, but the people who produced it have actually demonstration videos of many different types of catatonia, all the catatonic symptoms, how to elicit them from the patient. So this is a very valuable resource. Thank you, Dr. Sheebok. I don't know if anyone in the audience has one question or two for Dr. Sheebok. Otherwise, we can move on to the next presentation. I'm going to give you 10 seconds. It's the rule in our hospital. Go ahead. I have a patient who has had recurrent catatonic episodes, typically in the summer. And I'm wondering if I should prophylactically increase her lorazepam, which she doesn't like taking because it makes her sleepy when she's well. It's not the only medicine she's on. She's also on, I think, Depakote and a tiny bit of aripiprazole. Yeah, I want to repeat the question. So it's about a patient who has recurrent catatonia in the summers. The question is if there will be room to prophylactically increase her lorazepam by the time she typically, the season she typically gets a catatonia syndrome. I'm assuming that this is a patient that's been identified with a recurring psychiatric illness. Psychiatric illness. Is she bipolar? So she's bipolar and she needs Ativan in maintenance to stay in remission? Oh, that's a hard one. I don't actually really know the answer to that question. I don't really know if anybody knows the answer, but I would imagine that it might make sense to start giving. If you know someone is bipolar and you know they get catatonic when they have an episode, why not start to give them Ativan early? I mean, in the old days, people would sometimes treat manic episodes, you know, would give Ativan anyway for people who are manic. So I don't think it could hurt. I agree that it's not a question that has a known answer because it's a test where it's a study of one, an end of one, right? I think clinically, if you think of the risk and benefit analysis and you know that this typically happens, it might make sense to try and increase those, to run your own therapeutic test with her and see how she responds. I think it's a great case, yes. Maybe one more question and then we'll move on. Yes, go ahead. I have a case in mind that comes to mind. There's a patient who, in community, displayed early signs of delirium but it wasn't really detected. Treated as kind of BPSD with Risperdal and then that looked to worsen the delirium. The patient became rigid. Would you consider that catatonia until proven otherwise? Because I guess one of my supervisors kind of jumped into the conclusion that maybe there was an underlying Lewy body, but maybe we should have done the test there. The challenge, I mean. I'm going to try to repeat the question, if not I'm gonna ask help from you. So it's a patient with delirium that when you treated them with risperidone, they became rigid. And the question is, was this catatonia? It looked like it worsened the delirium, the behavior as well, yes. Yeah. Larry, so that's a question. So a patient with delirium treated with risperidone became rigid. Could this be catatonia? I wouldn't, the answer I think that I would give wouldn't be specific to delirium, but I just know from patients on, inpatient psychiatric units, anybody who starts to get worse when you're giving them more and more antipsychotics, then you have to start thinking catatonia, then you have to start thinking of what's causing it. So people who just, if people get worse on antipsychotics, then it should probably be on your radar, I think. Yeah, I agree. I think the general idea is to remember to keep catatonia in the differential. So we think it could be NMS, could it be just Parkinsonian rigidity right from risperidone but to increase the awareness to catatonia as a differential, I think. Very good. Yeah, I have a quick question. One minute for this question. Yeah, in the university practice and the clinical practice, I personally noticed IM lorazepam seems to be more effective for the challenge test than the IV lorazepam. I don't know, is it because of the IV fluids that they're getting? Let me see if I understood. Dave, you were nodding, so if not, I'm gonna ask for your help. So the question is, IV lorazepam being more effective than permanent? IM lorazepam seems to be more effective than the IV lorazepam. I see. In my clinical practice and the university practice, I don't know if it is because of the IV fluids that they're receiving, that they're not responding to the IV lorazepam, that they respond more to IM lorazepam. Okay, that's interesting. So I think, go ahead. I'll let Dave answer. Yeah, so the question is, why does it seem phenomenologically that sometimes IM would respond better than IV when sort of the teaching is that IV has better penetration than IM, which has better penetration than PO? I think the suspicion there, I would agree with you that maybe there's a dilution factor if it's being put in a bag as opposed to being sort of pushed at the bedside, which is what we typically recommend. I'll have the nurse push it and then page me, and then I'll go see them maybe 15, 20 minutes later to see how they respond. But yeah, we typically lean towards IV if they can push it. Thank you. Can you hear me? Okay. So I'm going to talk about delirious mania today, which will have features like of delirium, which was already was talking by Dr. Van Norstrand and also catatonia, which was talking by Dr. Shibbuck, in addition to some of the other features. I have no financial disclosures to make and this talk will include some of the off-label use of medications which are not FDA approved. Let's start off with a case that we have seen in our CL surveys. We had a 34-year-old male with a history of bipolar disorder type 1 presented to the emergency room with symptoms of hyperverbal speech, decreased need for sleep after stopping lithium due to chronic kidney disease from the lithium use. His outpatient psychiatrist started him on erpiprazole to replace lithium, but he still relapsed into mania. While he presented to the ER, he was very agitated, eventually required four-point restraints. He was continued on erpiprazole while in the ER and was also started on Depakote. He was also getting PRN or lamsepine in the ER for agitation while the bed search was in progress. While in the ER, while the bed search was in progress, on day seven to eight, he became very disoriented, confused. He was urinating inappropriately, pulling off his diaper and very labile with memory lapses. He also was not responding to the antipsychotics or mood stabilizers he was getting. So we'll talk about delirious mania, some of the signs and symptoms, assessment and management, and then go back to the case, okay? So delirious mania is a syndrome characterized by rapid onset of confusion, mania, with or without psychosis, and also some of the catatonic features. Clinical onset and course are notable for acute onset and rapid progression of symptoms, like within hours or days, and fluctuating course that alternates between psychosis, catatonia, and manic features and delirium. So there is a lot of controversy about proper nomenclature in the literature for delirious mania versus lethal catatonia versus malignant catatonia versus excited catatonia. And there is, this particular diagnosis has not found its place in DSM yet, which we'll discuss in detail in one of the later slides. Going back to the history of delirious mania, this syndrome received little attention in psychiatric literature. It was first described by Kalmel in 1832, but Luther Bell is the one who was credited for providing first comprehensive description of the syndrome in 1849. He reported 40 patients with the condition out of 700 admissions to the McLean Hospital. Krapplen, on the other hand, considered it as one of the subtypes of mania in addition to the agitated and delusional types. Fink and Taylor considered it as a form of catatonia. They called it excited catatonia. So far, we only have few case reports available and few case series. Only 14 cases were reported from 2004 to 2018, and we don't have any long-term research studies done on this particular delirious mania. The presentation I am doing today, the information I'm discussing is also from the limited evidence we have. All right, talking about the etiology of delirious mania, obviously, as the name suggests, it's a mania, so the primary psychiatric etiology is bipolar disorder, but there are other neurological and medical etiologies which were reported, like metabolic disorders, like azithomia and hepatotoxicity, autoimmune disorders like lupus, anti-NMDA, encephalitis, some of the CNS infections, and paraneoplastic syndromes. It can also be induced by drugs, like steroids, hallucinogens, and stimulants. Again, there is no enough evidence to report what causes are more frequent versus others due to limited number of case reports we have. Talking about the signs and symptoms of delirious mania, as the name suggests, both the symptoms of delirium and mania have to be present. So coming to the symptoms of mania, they present with irritable mood, reduced need for sleep, pressured speech, racing thoughts, distractibility, increased goal-directed activity, and impulsivity. As mania can present with psychosis, delusions may or may not present. Symptoms of delirium, like fluctuating level of consciousness, episodic confusion, episodes of incoherent speech with periods of lucidity, have to be present. Symptoms of catatonia, again, they may or may not present, and if they do present, they may present alternating with manic symptoms. And when they present, they present with negativism, mutism, posturing, grimacing, stereotypy, echolalia, and echopraxia. Catatonia, especially when it presents with agitation, which we are talking about exercise catatonia, can very much look like delirious mania, and they are overlapping syndromes, and it's very hard to differentiate. Talking about the assessment of delirious mania, we don't have any standardized diagnostic guidelines so far. DSM-5 does not include delirious mania as a diagnostic entity. It is not listed as a subtype of mania or delirium or catatonia. The hyperactive delirium, specifier of delirium in DSM-5 has a description similar to delirious mania, but it doesn't really talk about any catatonic features. Catatonia in DSM-5, describes agitation being a possible symptom, but there is no clear mention of mania in that particular subtype. Manic episodes in DSM-5, there is description of diagnostic features mentioning speech can be disorganized, incoherent with flight of ideas, and that patients may also display psychomotor agitation, but again, this specifier or this type doesn't talk about delirious features. So as we were telling, we lack formal criteria to separate delirious mania, excited catatonia, malignant catatonia, and lethal catatonia. Some of the clinical features we can try to notice while assessing for delirious mania are vital signs. Fever, hypertension, tachycardia are common, but again, they're not always present. Some of the unique examination findings, again, when I say unique examination findings, these are only found in couple of case studies. Acute onset, incontinence, inappropriate toileting, disrobing or extended periods, and pouring water on the floor or the head. Some of the bedside tests that can be done are gross errors on draw clock face, mocha, CAM, Bush-Francis scales, all of them can be administered, but again, depending on the clinical scenario of the patient it's hard to assess if these tests can be performed or not, always. Lab workup to rule out medical ideologies can include CBC with differential, CMP, urine analysis. We can also do CPK, blood cultures and urine cultures if fever and rigidity are present. Additional tests are only required if there is a clinical indication and some of them are EG, ABG, serum drug levels, serum folate, vitamin B12, serum albumin, iron studies, thyroid function tests, chest X-ray, EKG, LP, neuroimaging, like CT and MRI, and other blood tests, again, if there is only a clinical indication. One of the crucial things the clinicians must be vigilant is to rule out neuromedical ideologies of delirious mania because it's commonly seen with some of the autoimmune and paraneoplastic conditions as we discussed before, especially the anti-NMDA encephalitis. Some of them can be lethal, so it's always important we rule out medical ideologies before jumping into psychiatric ideologies. Management. ECT is the mainstay of treatment, but there are pharmacological agents as well, especially metbenzodiazepines, lorazepam in high doses. Most of the antipsychotics do worsen the clinical scenario due to risk of NMS. Typical antipsychotics are definitely contraindicated. Mood stabilizers and typical antipsychotics can be continued after the acute episode is over for maintenance therapy of primary mood disorder. Anticholinergics are contraindicated because they can worsen delirium. Talking about the psychopharmacological management of delirious mania, despite delirium being one of the core symptoms of the presentation, these benzodiazepines are the mainstay of treatment. Under lorazepam challenge, usually we start with the two milligrams. IV is the easiest way and probably the faster way to get the clinical improvement, but however, oral and IM formulations are also potential options. If there is no effect, the same dose can be repeated within three hours and again with another dose in three hours with the target dose of at least six milligrams in 24-hour period. And if there is favorable response, even the dose going up to 20 milligrams in divided doses is recommended in one of the studies. Obviously, since we are giving high doses of benzodiazepines especially with the patients having delirious features, close monitoring for respiratory suppression and paradoxical worsening of confusion is recommended. ECT, when there's no improvement with the medications, ECT remains the mainstay of treatment. Usually, improvement is seen within two to four sessions, but sometimes patients may require up to 12 sessions. Bichamperol has shown to be most effective rather than unilateral ECT, but obviously it is associated with more prominent cognitive side effects. All right, let's go back to the case. So this patient we discussed was a 34-year-old male present with a history of bipolar. Lithium was stopped because of the CKD and he was started on erythropresol, still relapsed into manic episode, but started on Depakote and also lansipine for agitation, but was not showing any improvement. In addition, started to show some signs of confusion, memory lapses, in addition to all the manic features. So going to the labs that we've done, CBC with differential, he had low hemoglobin and RBC. CMP obviously showed elevated BUN and creatinine because he had CKD. EKG was within normal limits, vitals were within normal limits. So clinically, we didn't have any other indication to do any other imaging or further blood workup. And so delirious mania was suspected. He was started on the lorazepam day nine in the ER, untitrated up to two milligrams four times a day, slowly in a few days. Erythropresol and lorazepine PRN were stopped due to concern of NMS and also because he was not showing any improvement with the clinical presentation. After starting the benzodiazepine, he started to improve after a few days. No IM injections were required for agitation. He was continued on the Depakote, which was started initially while he was improving on benzos and the dose was titrated slowly up to 750 milligrams three times a day. But he continued to exhibit disorganized behavior despite partial improvement of his delirious mania and he was eventually transferred to the inpatient psychiatric unit on the day 29 in the ER. Was eventually stabilized on carbamazepine in the inpatient unit and discharged. He continued to follow with outpatient psychiatrists and as of December of last year, he was stable on carbamazepine 400 milligrams in the morning and 600 milligrams at bedtime. All right, that's the end of my presentation. I have a couple of questions. Please select the correct statement regarding the syndrome of delirious mania. One, schizophrenia is the most common etiology. Two, delirious mania is a syndrome that combines symptoms of delirium mania but also present with symptoms of ketotonia. Antipsychotics consistently demonstrated better efficacy than ECT in the treatment of delirious mania. Antipsychotics consistently demonstrated better efficacy than benzodiazepines in the treatment of delirious mania. Right answer. Yeah, so as we discussed, the evaluation of patients with delirious mania should include ruling out potential medical and neurological etiologies. Bipolar is the most common psychiatric disorder associated with delirious mania. The presentation may include severe mania, psychosis, confusion, and symptoms of catatonia. The first line of treatment of delirious mania is benzos. ECT is reserved for people, those who do not respond to benzodiazepines. Question two, what medications are contraindicated or best avoided once delirious mania is suspected? Choose two, benzodiazepines, anticholinergics, antipsychotics, mood stabilizers. Yeah. So like we discussed, anticholinergics are contraindicated because they can worsen delirium. Antipsychotics are contraindicated due to risk of NMS. There's no absolute contraindication to stop mood stabilizers unless warranted for ECT, if that needs to be done. So coming to the summary of the presentation, delirious mania is a challenging syndrome to diagnose. High level of suspicion is needed when patients are presenting with both features of mania along with delirium. Usually the symptoms tend to worsen or have minimum response to antipsychotics. Benzodiazepine challenge is usually helpful for both diagnosis and treatment, but ECT tends to remain the mainstay of treatment. It's very important that we rule out neurological and medical etiologies because some of them can be lethal. And bipolar disorder remains the most common psychiatric etiology for delirious mania. Thank you. Thank you, Dr. Venigala. And we're going to open now for questions and answers to Dr. Venigala and the other speakers. Thank you. Hi, thank you so much for that very stimulating talk on excited catatonia delirious mania. Can you speak towards the challenges a little bit of getting someone through the evaluation process, especially when you're trying to consider things like EEG or an MRI scan and they are deliriously manic, peeing all over the place, disrobing, all those kinds of excited symptoms that you described, especially because you can't use anticholinergics, you can't use antipsychotics, you're left with benzos, but if you give someone a benzo and you're going to put them through an EEG, you may not actually get a seizure. Great question. The reality of clinical practice for these complex cases. Who wants to give it a first pass? I mean, like I mentioned in the presentation, yes, it is hard to do most of the tests with the cases, but if it's clinically warranted for a EEG, I'm not sure maybe we can do it when the patient is, and like you mentioned, yes, giving benzodiazepine and sending the patient for a EEG may definitely confide the results we would expect, right? Thank you. So it's hard. Yeah. I would just add that in this particular case, the patient had already sort of worsened while they were in the emergency room and they'd already been medically cleared. So we had labs, we had sort of initial data, and then it was really the worsening in response to antipsychotics that really elevated that in our differential. Yeah. You were able to keep a patient in the ER for 29 days and not get them admitted to the medical unit? That's impressive. It's challenging, yeah. The ear doctors would be like, admit, admit. I want to briefly, sorry for interruption, for the audience online, we are going to answer your questions via text after we are done with, because there are many people here waiting for their questions. So we're going to get to all the questions online later. Go ahead. Hi, I'm from New York City, and I've worked at the interface of HIV infection and mental illness forever, since the beginning of the epidemic. And one of the frustrations I've had is trying to help medical providers know when not to refer to psychiatry. I've also done international work, and I see a lot of people who die because medical providers don't recognize when a patient has delirium, send the patient to psychiatry, and it's completely inappropriate referral. So that's been a major focus for me, but I wonder how each of you approach that, because I tend not to think that a psychiatric etiology is as important as a medical etiology, only because my first goal is don't let the patient die. So I always start with don't let the patient die, look for what's medically wrong, even if there's a history of psychiatric illness. I wonder if you'd like to comment on that. I can start, sure. So the question is around referral to psychiatry when really there was something sort of medical going on. I think my point in my slides was around us as psychiatrists feeling free to say this isn't psychiatric, and not feeling sort of a burden to find something that isn't there, that in fact saying this isn't psychiatric or this isn't primarily psychiatric, except for sort of the impact of that thing on their mental health, is a valuable part of our service. So. I think what I want to add to that is that consultation liaison psychiatry has that elderly liaison part of it, and a lot of what we do is collaborate and educate our colleagues. So I think that's a very important part of our role. So we may get quote unquote wrong counsel sometimes, but to some extent one could argue they are never wrong, right? Because they see something, it looks behavioral, they think it's psychiatric, but they forget that medical disorders also can have behavioral presentations. So that part of education is part of what we do, I think. Please go ahead. Hi, my name is Esther Kelly-Cook, I'm from Houston. My question is. If you can please speak up, and everybody when they ask. Yeah, sure, I'm Esther Kelly-Cook from Houston. I had a couple of observations and then a question. So in Parkinson's disease, a lot of times you see REM sleep behavior disorder beforehand, and then you treat that with benzodiazepines, and also that can get a lot worse with neuroleptics. And I'm wondering, besides the dopamine connection, have you run across anything of a shared pathophysiology between Parkinson's and catechonia? Do you want to answer that? Oh. So the question is about Parkinson's disease, how sometimes presents first with behavioral manifestations before the motor symptoms, and for catechonia, that relationship, if you have found anything about a disorder of the dopamine metabolism in catechonia. I hope I gave, I did justice to the question. So the overlap I see is that you're talking about two disorders that get worse when you give them dopamine blockers. And get better with benzos. Right, so I didn't hear the part, I apologize, that also the REM behavior disorder responds to benzodiazepines, as catechonia does, right? I think, you know, so in the review, there is role for dopamine, there is role for GABA, right, in catechonia, as well as in those disorders, so there is some relationship. We don't know the detail of the relationship, but the answer is yes. In terms of the presentation of Parkinson's disease as behavioral, that also emphasizes the role of dopamine in depression, not only psychosis, right? So these syndromes are connected. I think it's important to remember the concept of syndrome, because even within catechonia, you are going to see very, very different presentations, and you are going to call both of them catechonia, but the pathophysiology of each one of them will be very different. Next question, please. Sure, I have three quickie questions. One, first of all, thank you for a nice lecture. It was very enjoyable. First question is, are you seeing delirious mania or your idea of it, is it more of a separate diagnosis, or do you think it more is it a subtype of catechonia mania? So it's hard to say if it's a subtype of catechonia or it's a separate entity. It looks like it's similar to excited catechonia as I was talking in my presentation, but again, there's no clear diagnostic formulation or description of anywhere to have a standardized guideline to look up if it's a subtype of catechonia or if it's a separate entity. So second quick question is, I'm a program director and I'm trying to train my residents how to treat catechonia, and I often feel that they go gun-shy on giving Ativan. My usual doses for this is somewhere between six and 16 milligrams in divided doses. I'd like to know if you have similar situations. I mean, I beat up on my attendings who tell me that they've got one TID and nothing's getting better. So I think you really gotta go all out with the Ativan. I don't know if you have similar experience. The dosing of flogastepam for catechonia, how is the typical schedule and the dosing? I think part of it is, yeah, how much do we, are we aggressive enough, really, is the bottom line. Do we commit to it enough to really rule it in or out? I think some of it is a pragmatic challenge of by the time you get to that second or third dose, it's late in the day, do I wanna give this additional two milligrams and then leave for the day? I know that's part of the problem. We probably could be more aggressive. What would you say, Larry? I know of some cases, but actually, almost like more in the pediatric literature, where it's kind of more critical to get the patient out of the catatonic state, where they've gone to very high doses and it is described. But I think we're all kind of a bit queasy about keep giving higher and higher doses in a general hospital, because we're the consultants. But the other thing in terms of giving Ativan, I wanted to think is important to mention, and I learned this from my training directors, if you're gonna give somebody Ativan for a challenge, go back and talk to them in an hour or see what they're like in an hour, because that's really the classic way to evaluate what I think the Ativan challenge is all about. In other words, if somebody really has a classic response in an hour and they can talk to you, it's important diagnosis, but it's also, they'll talk to you and then they'll give you the diagnosis sometimes, because you can get a history at that point. And my last question, we're, you know, catatonia sometimes is a post encephalitis. Are you seeing an uptick in catatonia in a post COVID world? It seems that way where I am in my hospital. We had, for myself, we've seen deliriums and psychosis post COVID, but I'm not aware that we've seen specific. We have not seen it in our service personally. Yeah, yeah. I wanted to very briefly talk about your previous question about delirious mania. The reason why we wanted to discuss this syndrome is because of how controversial it is and to raise awareness about it. In terms of the etiology behind the syndrome, we had a discussion even among ourselves where, you know, some authors consider it typically more a syndrome of bipolar disorders, while other authors will emphasize more, look for immune encephalitis, look for the medical reasons. So it's a very controversial topic. And the question is, should we even use that terminology, right? We felt that there was enough clinical interest, right, to bring it forward for increased awareness when somebody has that intersection of catatonic features and manic features and delirious all at the same time. So that's why we were curious about it to continue reading about it, about this gradual progress we make in medicine and psychiatry. Thank you. Go ahead. I just had a quick question. On the first case. Oh, go ahead. I think we often are taught to identify the underlying cause of the delirium. In this particular patient, 63 years old, with chronic benzo years, 4 mg QID, as you mentioned, was the differential in terms of the cause of the delirium, benzodiazepine withdrawal? And if so, did she have features of benzodiazepine withdrawal during the time that she was delirious? And if so, and then the third question is, if it was not benzodiazepine withdrawal, if it's new onset seizures, was that part of the delirium being postictal? Yeah, so the question was really sort of the ideology of this particular delirium, given that she was on essentially 4 mg a day of clonazepam. We suspected, and I think I may have mentioned this, we suspected that she had withdrawn somewhat from her benzo, that she had maybe missed, was unable to refill it, had run out maybe a day or two before this presentation, and so that this was, in fact, an induced seizure that she had that caused her initial car accident, and that what we were seeing primarily was postictal delirium, in part because, and we didn't see a lot of the other signs and symptoms of benzodiazepine withdrawal, because I think to the primary team's credit, they put her back on sort of a lower dose, but they put her back on her clonazepam pretty quickly, in part because she was having seizures, and so they put her back on her home clonapin, and so we sort of weren't able to definitively answer it for that reason. I think we counted it a win that we sent her back to her home prescriber on a slightly lower dose for chronic benzodiazepine. Thank you. Thank you, I have just two quick questions. Danielle Kushner from New York City. I work in correctional and forensic settings. So one first point about the delirious mania, when you were presenting it, and I'm not in CL settings as much, that I was surprised and interested, and it sounded very similar to K2 presentations that I've seen, and I'm curious. I'm sorry, to what presentation? K2-induced psychosis, in that they have so much mania that's present, and people become delirious as well, depending on their presentation, and whether you guys have seen that similarity, and also any overlap. I found in my treatment of K2 psychosis, they respond better to atypicals. So there seems to be some overlap there. I personally have not had any experience of seeing or treating any patients with K2 psychosis, and personally, this is the only case of delirious mania I've seen in my experience. So I don't know if any of my panel has to add any more comments. I've seen a number of K2 psychosis on an inpatient unit. They just behave so crazy, and they don't have all of the classic motor symptoms of catatonia, or either the kind of not responsive or ovary symptoms, just absolutely crazy behavior. But when it was K2, it goes away. It's a longer psychosis than other substances, but eventually it resolves. Yeah, I haven't seen as much catatonia, but I think definitely with the bipolar mania aspect of it. I'm relieved. I thought you were gonna ask me about cancer syndrome, which you've probably seen more than I have. So my last question is in the presentations of catatonia that I've seen in correctional settings, and just the biases of different providers of not thinking that they're catatonic. A lot of it has been mutism, staring episodes, but people are still walking around and agitated, assaultive, and sexually, abnormal sexual behavior is intrusive. I'm curious if you guys have any tidbits or any antidotes, especially in trying, I try very hard to educate this to both hospitals that I'm sending these patients to and my other treatment providers to recognize this, because they're usually eating a bit, and then they think once they're stopping eating, then they're sick enough and catatonic, and it's just a struggle in my setting. Thank you. The two things that staff, when it's ended up being catatonia, the two, or one of the most common things that the staff will tell you is that they're not eating, they're not talking, they don't say anything, they're just not interacting, and then when you look closer, that's one, but the other time where it becomes worthwhile to look is patients, there was a patient on a unit I was on that was a little bit like Hema's, a bipolar patient, and just more and more, and he responded to antipsychotics in the past, and mood stabilizers in the past, but on this admission, just kept getting worse and worse and worse and worse with more antipsychotics, and then he was lordly delirious and manic at the same time. We are actually over time. Thank you very much for your attention. Those of you who have questions, you are welcome to approach the speaker. Thank you very much. Thank you.

neuropsychiatry

consultation-liaison psychiatry

delirium

acute psychosis

catatonia

delirious mania

differential diagnosis

Ganser syndrome

Lewy body dementia

bipolar disorder

lorazepam

ECT

psychiatric disorders