Psychiatry & Psychotherapy Podcast - Catatonia in Children and Teens

Episode Date: June 27, 2025

Catatonia in children and teens is underdiagnosed, frequently misunderstood, and potentially fatal if left untreated. In this episode, Dr. David Puder and Dr. Annabel Kuhn interview Dr. Joshua Ryan Smith—child and adolescent psychiatrist and division director at Vanderbilt University—to explore the essential clinical skills and medical knowledge needed to identify and treat pediatric catatonia. You'll learn how to differentiate catatonia from other neuropsychiatric conditions in both neurodivergent and neurotypical children, how to apply tools like the Bush-Francis and Pediatric Catatonia Rating Scales. This episode also unpacks common misdiagnoses in cases involving autism spectrum disorder, schizophrenia, and autoimmune or metabolic conditions. Finally, it offers practical, evidence-based guidance for both inpatient stabilization and outpatient follow-up care. Whether you're a psychiatrist, pediatrician, therapist, or student, this episode offers life-saving insights into one of the most overlooked syndromes in child psychiatry. By listening to this episode, you can earn 1.0 Psychiatry CME Credits. Link to blog. Link to YouTube video.

All right, welcome back to the podcast. I am joined today with Annabelle Cune, MD fellow in Boston, child psychiatry, also with Joshua Ryan Smith. He is a C&L child and adolescent psychiatrist who has published on Catatonia and autism. And today we are going to be talking about both and mostly Catatonia. And so, yeah, welcome to the podcast. Thank you. I appreciate the invitation. Yeah, I was enjoying listening to your YouTube the other day. And just for someone jumping in, what is Catatonia? Like, what are the general symptoms? And then what are the specific symptoms we see in autistic patients?

Sure. So Catatonia, you know, was described in the late 1800s by Colbaum initially. And it was described as this sort of stuprous tension and sanity. And they also described fluctuating levels of psychomotor activity, right? I think that's like a hallmark of, of catatonia where people have either hypoactive symptomatology or they have hyperactive symptomatology. And it is a syndrome in the sense that catatonia always

occurs in the setting of something else. The analogy I give to parents and families is a catatonia is like fever, right? Like you have a fever, we don't really know why you have a fever, but you have a fever and we can treat it with ibuprofen, right? And that can happen in catatonia. We sometimes know why someone's catatonic, like in the case of an MDA receptor and stuff

which is probably the most commonly associated medical condition with catatonia and then we can treat end ender receptor incephalitis right steroids you know retuxumab you know the full court press in terms of in terms of treatment options there which improves the catatonia and the encephalitis but in some cases you don't and you can have psychiatric symptoms that cause catatonia so the most common of which are schizophrenia and bipolar disorder in kids psychosis seems to be the most common underlying psychiatric eadology for catatonia and adults that is more likely to be mood disorder for bipolar disorder. And then you have these, again, these sort of underlying medical causes for the catatonia. As you were talking, I was starting to think about delirium because this is another diagnosis

that is fluctuating and associated with another diagnosis. And so when you see, when you approach a case where you're witnessing fluctuating symptoms and potentially associated with another diagnosis, how do you really differentiate delirium from catatonia? That's a great question. I mean, the DSM separates them out and says they can't occur. They can't be comorbid, but they certainly can. And it's really challenging. When we have folks who there's catatonia and comorbid delirium, we use our catatonia assessment measures, which I sort of already talked about, right, the Bush Francis, the canter. But then we use the Vedic, so it's the Vanderbilt. So this is for kiddos specifically. So it's a Vanderbilt assessment for delirium and infants and children.

And we use both of those and try to basically assess for each. And again, back to the physical examination findings. Physical examination findings are like absolutely critical in delineating between delirium and catatonia. So if you have somebody who has waxy flexibility and they're stuporous, they're more likely to be catatonic if they're stuporous and inattentive without waxy flexibility, right? And the treatment plan is also kind of challenging, right? So when you have somebody who's delirious, hyperactive delirium, for example, the standard operating procedures to use antipsychotics. Well, anesthetotics worsens, worse in catatonia, right?

And so you have to be really cautious around. How do you delineate the... But when we first started talking delirium is what I thought of, too, is that I think it is probably the most analogous condition in terms of, you know, the acutely altered mental status due to an underlying etiology. Okay. So what are the most common physical exam findings that you're following and watching? Yeah, I think, so back to your initial question around the catatonia-specific symptoms for kids and adults, right, and how those delineate. So when you can have hyperactive and you can have stupor's catatonia, and we haven't really, as a field, documented what are the most common symptoms, but the ones that are captured in the DSM-5 and the Bush-Francy. I think, you know, are all something that should be part of the assessment.

So you have, so for the soup, the stuporice iteration, you have waxy flexibility, reduced oral intake, you know, reduced fluid and food intake, reduce verbal communication. You either have, again, either stupor or, you know, excited levels of activity. Aggression is also a potential symptom of catatonia. It's on the Bush Francis. It's also on the canter. increased impulsivity, reduced, poor eye contact,

fixed gaze, new grimacing mannerisms, so odd movements that don't seem to have a goal. And stereotypies, the repetitive movements. And when you start looking at pediatric cases, though, so for kids, the most common symptoms of catatonia are reduced verbal communication

and reduced oral intake. Would that be like the stuporous iteration of catatonia? Well, so yes and, yes and a little bit there. Because catatonia is a life cycle illness, right? So it can happen at 6 to 96. But the younger you are, the more likely you are to have catatonia due to a neurodevelopmental disorder like autism. And if you have catatonia from a neurodevelopmental disorder, you're more likely to have hyperactive symptoms of catatonia.

Do you think that it's more likely to be a sort of, associated with a neurodevelopmental disorder in kids because psychosis, schizophrenia is less, and even depression is less common in kids than adults. Maybe we don't really have the data to be able to demonstrate that. I think there's a lot of interest in why is there a connection between catatonia and autism? What I can tell you is that based on really large data sets that we've done our analysis on, is that kids, when they have catatonia are more likely to have a neurodevelopmental disorder when they have the diagnosis earlier in life relative to you're probably right but there's there's also probably some

sort of underlying biologic susceptibility to catatonia earlier in life if there is a comorbid neurodevelopmental disorder that we don't fully recognize and so that you know i think it's still to you know be researched and explored in greater detail how common is this in autism patients like that you follow in your clinic and yeah maybe you just start with that one yeah it's more common than we thought it was initially there's there's a great meta-analysis uh by vikirzo serrano i think was published in like 22 european psychiatry where they speculate that the prevalence of catatonia autism is 10 to 20 percent or 10 to 12 percent of folks with autism will have catatonia across the course of their life at some point and there are there are folks to argue again

that because vicarious astronomers metanalyst primarily included inpatient samples and that's that's fine but even if it's 5% or even if it's 3% that's still a significant number of people who are having a very severe psychiatric syndrome that is a hard to recognize but is be treatable if identified take me through the time course like let's say there was an autistic kid what would be the first symptoms that normally come up with catatonia and the second and the third and the fourth like what is that what is the time trajectory of this? So when you have somebody who has autism, there's generally that initial early life regression, right?

That's more sort of prototypical for an autism diagnosis. Like two, around two or three, they have been normally developing, and then they fall off their developmental trajectory and then try to get back as close to their developmental trajectory as they can, right? As they get older, if there is a second regression,

that's when I start queuing into, is this catatonia for somebody who has autism. So that really any age past four or five. And so what you're looking at is, you know, limited engagement, a loss of personality, loss of ability to accomplish ADLs is another really big one. Some kiddos, like, they'll go from brushing their teeth to not being able to brush their teeth at all

and they need to like have folks prompt them or move the toothbrush for them. Reduced eating, reduced drinking. That's what really increases the mortality risk, especially. But then in neurodivergent folks, in folks with autism, there's also this reported elevated rate of aggression without like an antecedent necessarily. It's just aggression that's happening in space without prompting or this automatic self-injury that's not, it's not trying to, it's not a way of communicating with someone, right? So it's self-injury that doesn't have necessarily a purpose. And so those symptoms are the word store what starts to cue me into this may be catatonia in a, in an, in an,

autistic individual who's early in life. And we've identified folks as early as four, where it's like they've had their initial regression, they're getting back, and then they have a really big regression and have those sort of symptoms clusters that we followed in clinic here. So for kids who are past beyond the age of four and having these behavioral regression symptoms, that would really perhaps could indicate to a clinician that this might be catatonia more so than if it were to happen, like before age four. But I just wonder, are there other besides the aggression and irritability and loss of skills after age four, how else can Catatonia be differentiated from behavioral regression or skill loss in autism? Yeah, again, it comes back to the physical examination findings too. It is tremendously

helpful to be able to conduct a standardized physical exam like the Bush Francis or the canter and be able to, you know, because the differential is, and you sort of hitting on this, right, the differential is broad if you have someone who comes in with skill loss or if you have someone who comes in with irritability that can be depression right that could be other mood symptoms it could be psychosis you know so on and so forth but if you have those symptoms the presence of physical examination findings that's certainly queuing you in so i imagine that it would be really hard for a telehealth provider to examine someone with catatonia is that fair to say actually um we we just published a paper a year ago where we looked at the sensitivity of assessing somebody with catatonia over telemed.

And if you can get the family to engage in the Bush Francis, the sensitivity remains pretty high. It's like 98%. Wow. So, and I do a lot of telemedicine visits, and it asks a lot of the family, for sure, but you can send them videos. I know you guys have had Dr. Oldham on here. Like, you can send them Dr. Oldham's Bush Francis videos and have them review, and you can actually have the family do it in real time. So telemedicine is actually not an unreasonable way to assess folks in the community.

With the nonverbalness in some autistic patients, how do you determine some of the mutism? It's not captured on the, it's basically losing what communication ability they have, right? Which is not captured on the Bush Francis or the canter. So a classic example is somebody who uses an AAC device, like they're using artificial communication, and then they stop, right? Or they're nonverbal and they sign and then they stop signing. And generally what I've seen in clinic

is that's also accompanied by a virginiburation, so the nonsensical noise production. So even if someone's nonverbal, they go from, we'll say someone's limited verbal, say they have 30 words, right? So they'll have 30 words, that drops off, and then they try to communicate with nonverbal gestures,

and then that drops off. And then they usually engage in screaming or some other sort of distress. sounding vocalizations that we would call Vigibration in the studying Catatonia. Okay, you said something else that was interesting. You said, like, the type of violence is different between Catatonia and maybe just autism with violence?

What is the difference between the two? Yeah, this is a particularly big area of interest for me because I take care of mostly folks with profound autism, and I want folks to consider Catatonia on the differential when there's worsening aggression because it's a treatable cause of aggression and there's so many causes of aggression that aren't treatable, right?

And it's just the severity and nature of it is really devastating to families. And so if you can intervene and treat those things, it can make a big difference. So when you have somebody with profound autism, it's not uncommon that they're aggressive, right? Like, that's not unusual.

But the question is why? And then also trying to assess for the severity and frequency. So if a kiddo is aggressive, but they're aggressive because their parents are taking them in a place they don't want to go, that's different, right? That's the kid communicating. I don't want to go to this place, but they don't have a good way of communicating, particularly they're minimal verbal, minimal verbal or nonverbal, right? Or self-injury is the same way. So if a kid doesn't want to go to bed and they engage in self-injury, that's communicating to the parent.

I don't want to go to bed. The levels of aggression and self-injury that you see in Catatonia are they're not driven by something like that. they're not driven by like a cause and effect. They're just happening all the time and they're sort of indiscriminate. I think we've had families who say, you know, we can't even go to the grocery store because if our kid passes somebody else, they'll attack them, right? Or they're just engaging in self-injury nearly from the moment they wake up to the moment they fall asleep and there doesn't seem to be a rhyme or reason.

So that's the, that's a differentiating factor there, right? It's both intent, cause and effect, but also the intensity, severity, and frequency of when it's happening. It's really good. What are some more pearls about the diagnosis that you would want clinician's done to know about that they don't know about? Well, I think that, again, you know, considering Catatonia on the differential, I think, is really key. Because what happens sometimes, too, is you can also get, we haven't really talked about negativism or oppositionality in Catatonia, right? Which is a cardinal feature of Catatonia, where folks will either can't do what's asked of them or they do the exact opposite. It's close. active negativism. It's like the most severe iteration of that, right? But it can be misconstrued as oppositionality from a kid who just presents the emergency department. So if you have a kid who previously was following instructions to their family just fine, and then the next day or a week or a month later or something like that, they can't do any of those things or they don't seem

capable of following directions from their family, you present to the health system and folks are like, well, you know, they're just being oppositional. They don't want to be in the ER, so on and so forth. It's like, well, we need more information, right? I mean, that may very well, may be the case, but if we had a, if we can't do anything that we previously were capable of doing, then that starts queuing me into this negativism from catatonia rather than just sort of baseline oppositionality. And it's, it's easy to sort of falsely attribute a kid not wanting to follow instructions to just oppositional or not wanting to be in the hospital or not wanting to do with the adults telling them to do, right? And so, um, I think making sure that that's on the

differential is, is key as well when you see, again, a big departure in terms of personality. in terms of engagement or aggression or negativism. I think the big important pearls are, you know, it is a life-threatening illness. Oral intake can be reduced and that can be really scary. And a lot of these kids present to hospitals when they're not eating or when they've had, you know, their symptoms first occur. And then, you know, just go ahead.

Real quick, with the negativism, it seems like this is so vital because all of a sudden, the child is doing the exact opposite of what you're asking. Right. And it's like everything in you as a clinician is like, oh, are they just all of a sudden being rebellious? Right. You know?

And it's such a good differential. I just want to say that. And then the oral intake, not drinking, not eating, when does that happen in the course? Is that the first week these things start happening? Like, you know, like when do you usually see that happening? We don't really have good data on that necessarily, and it depends on the kid. You know, so we have some kids who've come in and they're floridly catatonic three days after the catatonic symptoms started, right?

And then we, and when I say floridly catatonic, I mean requiring IV hydration in G2 feeds. It's like, it's very quick. And in my experience, again, this is not as day driven as I like to be. But in my experience, that's generally in the case of encephalitis or first episode psychosis where catatonia is, you know, accompanying the acute symptomatology. What I'll say is that for more of our chronic catatonia patients who in our clinic generally have autism, the ones who have residual catatonia symptoms, the oral intake is the issue can come and go where it's like, hey, they won't eat for three to four days, then they'll eat for a day,

then I'll go three or four days. It's not as clear a delineating line as some of the other kids who have presented to the acute care setting. So it's difficult to know. And I think it also, I think, highlights the need to be really clear and collaborative with parents around timeline of symptoms.

Because if a kid goes without eating for a couple days, your differential is more broad than if they go without eating for a couple days, but they also have lost their personality and are not doing ADLs and are posturing, right? So just making sure that you're assessing

for all sort of factors of the particular symptoms. For clinicians who suspect catatonia in the outpatient setting, and let's say there's no poor, like, PO intake is intact, would you still recommend the family bring this kid to the ED? That is a great question. And my answer is it depends. So it depends on how severe the oral intake issue may be. And it depends on how quickly you need them to get a medical workup, right?

So it's really important when kids across the spectrum of neurodivergence or age present with catatonia to do a full medical workup, including brain MRI or LP, if that's clinically indicated, right? Definitely baseline labs, definitely physical exam, definitely having pediatrics weigh in. You know, and so the questions in my mind, if a kid presents to my office and has catatonic symptoms and they have not been assessed at all, like let's just say they walked in my office, see them here, they've never seen a doctorate. before in their catatonic. I would start atavan for sure. And in outpatient settings, on the inpatient setting, you can do the adivant challenge, right? Where you can go and give them repeat doses of adivant until they fall asleep and then reassess them. Outpatient is more complicated. So I generally start low and go slow and do three doses of adivant into like three doses per day, start at a quarter milligram, go up every couple of days. And then coordinate with the family, generally through

the my health system in on epic, around if they're sedative. at higher doses. So that's what I'll do in terms of pharmacology. If I see them here and they've never had any medical workup and they've never seen a pediatrician, they haven't been eating for a week, I will absolutely send them to the hospital for sure, right? It just depends on A, how much medical work of do you need based on when they're coming in and then B, how acutely concerning are their symptoms right now in terms of their medical stability? Is it the encephalitis that you want to rule out by sending them in? Is that the main thing? Or is there some just in a mixture of things? The answer is yes and.

I mean, encephalitis is certainly the number one thing I want to rule out because time is brain, right, particularly in encephalitis cases. And if a kiddo has encephalitis, we need to go ahead be doing steroids, monoclonia antibodies, whatever it is that we need to do. So yes, encephalitis is the number one thing. But, again, you can have catatonia from a myriad of different medical conditions, and it's really broad. And so you oftentimes need to do a lot of labs just sort of as a general assessment to make sure there's no sort of metabolic derangement or other medical ideologies

that are causing the catatonia. Okay. And so you said something, you give the out-of-in every hour until they fall asleep. Tell me more about that. Yeah, so that would be in the inpatient, heading out-patient. Just to clarify.

Yeah, yeah, yeah. I don't want anybody slinging that much out of me at how the... Oh, but that's still interesting. I mean, that's not how I've... Walk me through that. Yeah. Walk me through that.

What do you guys do? So we actually published a paper on this. It's called Roadmap. It's the Vanderbilt Roadmap for Catatonians and the JCLP. But basically what we do is we give an out-of-van dose, like an Al-A-Van challenge dose, with the max of two milligrams of At-A-Van for the single dose. And then we go back and reassess to see how their symptoms have improved.

And we repeat the Bush-Francis every hour when we go and evaluate them. So we give them two milligrams, and then we'll come back and give repeat doses based on their weight until they have, are you guys familiar, the Richmond Agitation Ced Cedation Scale? It's a, we use it in, so basically it's a lycard scale of agitation that folks use in the hospital. So zero is like not agitated at all. And then there's plus one, plus two, plus three, plus four as increasing levels of agitation. And then minus one, minus two, I think goes to minus five, but levels of sedation.

So we basically repeat the doses of Ativan until they have resolution of their catatonic symptoms or they have a rass of negative 1, which means slightly drowsy. So that's the assessment that we use. So we try to be pretty proactive. And that's an idealized situation, right? Like in reality, you're doing that and you're also being called to behavioral codes or getting doing a new console. You can't just be standing at the bedside the whole time. But that would be the idealized version of that. Okay.

So in this idealized version, what kind of doses? are we getting to in the first day, like cumulative doses? It depends on the kid. You know, we published a paper on the number of, the 150 kids that were admitted between Mass General and Vanderbilt and the mean dose of Ativan for those kids was six milligrams for stabilization of their catatonic symptoms. Per day. Per day.

Right. And so I think in the hospital setting and the acute care setting, thinking about it in that dose range is reasonable. But what I will say is that our clinic paper that focus primarily on folks with autism and catatonia, the mean dose of lorazepam was much, much higher. It was 20 milligrams. And so there's a pretty wide discrepancy

of what people need in terms of stabilizing their catatonic symptoms. But we try to follow the old adage of catatonia care where you continue to dose until sedation and then reassess. And what percentage of people do not respond purely or as much as you would want to add-of-in and you have to move to other types of treatment? It would be a guess, but I would say probably, I think 80% of people respond to Ativan, I would suspect. That's just a guess.

But what I would say, though, is that the majority of patients that we have followed longitudinally have needed more treatment than just Atavan, particularly our neurodivergent folks. So whether that's an NMDA receptor antagonist, like Mimantan or Amantadine or Deppocode or Closopene or E.C. the majority of patients we've followed longitudinally in clinic have needed additional either pharmacologic or neuromodulatory interventions. So for kids who have had a paradoxical reaction in the past to Ativan, and now they're presenting with Catatonia, how would you approach that situation? That's a tough one. It, again, depends on the severity of their symptoms.

So if they're coming in and they've had paradoxical reactions, and we have a couple of cases like this, if they are have intractable aggression or they're not eating or drinking, I'll usually go ahead and start pursuing ECT at that time. And then I would also simultaneously do Mimantin, an NMDAR receptor antagonist or depicote at that time. So that's usually my approach. Got it. Yeah, I would love to hear your thoughts of like if a kid isn't clearly like having a, let's say, for example, they're on 20 milligrams a day of Ativan, there's no clearly robust response to Ativan. What would you do from that point?

Like, what would be your next step? Have we pursued ECT yet? Not yet. Okay. I would have done ECT a little earlier. I think that I wouldn't let him get up to 20 milligrams. I would go ahead and start doing ECT if they're not responding at all. And, you know, that's tricky. I'm also the medical director for neuromodulation here. And the laws around electric and both of therapy are really variable from state to state. In Tennessee, if a kid needs ECT, you have to have two consults completed by one by a cap psychiatrist and then another one by the ECT doc. And then that's if they're 14 to 17. And if they're under 14, you have to do that. But then you also have to do a multidisciplinary meeting of five people and go to court and get judicial approval. And so that process can take a really long time.

So anyway, if someone came in and they were having that much, that level of subtatology at that dose of Bativan, I would do, I would continue to benzo. I'd start an NMDareceptor antagonist. I would start pursuing ECT. And then there's, there's an algorithm for it. There's a great paper by Beach in 2017 where he does an adult algorithm that I follow roughly, where it's benzodia's ECT, NMDA receptor antagonist, phalproic acid, and then either Araprizoal or clozepine as that sort of last line, because those are really the only two antipsychotics that have shown to be, you know, potentially efficacious and in catatonia.

Joshua, this is, this is first of all really, really helpful, I think, just putting this on people's roadmap. As I'm talking to you, I'm on X a lot, and there's a lot of anti-psychiatry people, and every time they say something anti-psychiatry, I just want to say,

do you know what catatonia is? Do you even know what catatonia is? Sure. And then that question makes me want to ask myself, how long until neurology steals this diagnosis from us? I think they're good. Yeah. Okay, good.

I mean, you know, watch turf. But, no, I think that they're okay. The fact that ECT is the, is one of the hallmark, if not the hallmark treatment for Catatonia. It's the only FDA approved treatment for Catatonia even. Right. It means that it means that Catatonia, I think, is in psychiatry to stay. my dear neurology friends, I don't think have any interest in cross-training

in ECT with us. Though if they do, I'm happy to accommodate them. But that has not been the case thus far. Okay, so if they did respond to Aduvan and they're out of Catatonia, they're doing so much better, my perspective is you treat the underlying issue, if there is one.

And then secondarily, my mentor taught me go down very slowly on the Atavan, like half a milligram once a month, which no, one knows that. So tell me what your perspective is and how you roll. I do the same thing. I am incredibly cautious around tapering benzodiazepines. And I go, it is, I tell the families I see in clinic, it will be so painfully slow. It will drive you nuts. But it's, I think it's critical

because the symptoms coming back is not what we want, right? Like we were in the hospital or we're, you know, severely debilitated secondary of the symptoms. So we have to be cautious. What, what is, there's not very much data on benzodiazepine tapering in the literature. We did include our tapering data in our autism and catatonia paper. And what we found was that we tried to taper benzodiazepines for 12 of our 45 patients. And we were only successful in absolutely stopping benzodiazepines for five of the 45 patients that we had in that sample. And so what that tells me is, I think we conceptualize Catatonia as an acute condition, and understandably so, right? People come to the hospital, they're acutely ill.

We do a benzodiazepine-channelcy to BCT, but there's just not very much written about what happens when you go to the clinic. I think tapering is challenging, and I suspect, I don't have this data because I primarily focus on folks with autism in Catatonia, but I suspect there's probably greater success in tapering to discontinuation for neurotypical folks with Catatonia relative to neurodivergent folks. And so, you know, that, but that question has to be answered. That's just my hypothesis. Yeah, that makes sense. And I'm surprised five out of, it was five out of 45 were able to totally take profit. Yeah, like there was one patient who I saw who is on a very high dose of

Ativan and is now outpatient getting ECT still on a very high dose of Ataband though. And anytime it's decreased by the even tiniest amount, like quarter of a milligram, things get worse. and he either has to go back to the hospital or a dose has to increase. And it's really unfortunate, maybe. But, I mean, if the treatment helps, that's great. But I think for parents who are, yeah, they're really concerned about having kids on this high of a dose of benzodiazepines. How do you coach parents or guide parents through the rationale of why we're prescribing such a large dose?

Yeah, and I'll also add that we run into that with ECT frequency, too. where it's like we try to taper kids to weekly or something like that and they just fall off. I coach families on that by saying, listen, we do not understand or fully appreciate the ramifications of taking Atavan for years and years and years. And there's also not longitudinal data on this. That's why we have this research clinic where I follow up with these folks. But my assumption is that it's better to be on AtaVan. and not be catatonic, then to be off of Ataband and be floridly catatonic for your long-term, for your long-term life trajectory, right? There is, you know, concerned that taking benzodiazepines

for years increases your risk for dementia, absolutely. But there's also, you have to be able to live your life and function and eat and stay alive. And so when you are looking at it and comparing those two options, it's hard, you know, and I really empathize with my families a lot around like what how do we make this decision together and collaboratively around what are you comfortable with your kid taking for how long and how low can we get them without any residual symptoms returning it's a it's a difficult conversation to have but it's absolutely critical what about a similar type of conversation how do you approach the option of ec t with families especially those families who have seen eCT in movies and are really hesitant didn't even know

that psychiatry still does ECT routinely. Yeah. It's a delicate conversation around, I frankly own the fact that ECT started off not with great marketing, right? Like we used to not use generalized anesthetic. We didn't use paralytics. You know, we didn't put people under sedation

and paralyze their muscles so they don't have a big herky-jurkey, tonic seizure like you've seen in the community. I also think one of the cuckoo's nest did a huge disservice to build ECT access, really. You know, because there was a movie everybody saw and the way it was portrayed, I think, has set ECT access back. But I will, I'll tell families, you know,

I'll say ECT's come a long way. Yes, the procedure is largely the same, but we have made changes to the procedure, including modified ECT where people are under sedation and paralyzed. And I also actually, I'll get really nitty-gritty with them where, and I'll tell them, like, as much detail as you want, I'll give you, where I'll talk about we move from sign wave pulses,

pulses to block wave pulses, and we can do brief pulse or ultra-brief pulse, that there's modifications that we've made that have improved the clinical outcomes and also the side-effect profile for ECT. But, you know, I walk through every kind of every step of the situation and what is what they can expect when they come in and get treatment. But, you know, so many of my families, when they eventually find me or see me, their kids have been sick for so long. They really just are saying, please, you know, anything we can do to get my kid, even you know, 30, 40, 50 percent closer to where they were, as close to their baseline as we can possibly be. And so I think just, again, being able to sit in that with them and talk about, like, this is a

really difficult thing for us to walk through together. But if we look at the data and we look at the literature, I mean, ECT has been used for children since 1940, you know, and so there's almost 100 years of data that supports its safe and efficacious use. That doesn't mean that it's not stigmatized. That doesn't mean there's not side effects, but just having a very very, you know, candid conversation about that sort of an all-fronts. I think another challenge that adds to ECT and Catatonia and kids with autism so often, not so often, but frequently a seizure disorder can be, can occur in association with an autism diagnosis. And so I would imagine that for a kid with a history of seizures, even if it's remote, it might make people hesitate to consider ECT. It does, but it shouldn't.

So you can actually use ECT to treat non-convulsive status epilepticus. There's protocols at various hospitals, not here, unfortunately, but there's one published, I think, by the University of Maryland, where ECT actually can improve seizure outcomes for people that have comorbid epilepsy. Now, I say all that with this caveat, you have to be absolutely really careful when you do it because folks with epilepsy are at an elevator risk for having prolonged seizures from ECT, and kids are at an elevator risk for having prolonged seizures from ECT. So if we're doing like a hypothetical scenario, if you have a kiddo who comes in, they have profound autism, catatotone, and epilepsy.

And this is not an uncommon sort of triad of diagnoses. Then what we do is we start as low as we possibly can on the energy from the ECT machine. And then we slowly up titrate it over time to see what that person's going to be able to tolerate. That's both efficacious, but doesn't result in prolonged seizures. The data is pretty clear that kids have longer seizures relative to adults at lower injuries. And so we have to be cautious about that. And then again, in the setting of the comorbid epilepsy or seizure diagnosis, it's a critical consideration.

So if Ativan isn't working, would you try a different benzodiazepine, like clinazepam? And has that seemed to be more helpful in certain situations? I definitely do. And I used to use diazepam with relative frequency, but I don't do that.

I usually either use loriasopam or clinazepam. That's my own comfort level. that's not as data driven. We have published papers on the use of clenazepam. And actually I started using clenazepam. It was a little bit of a happy accident during the Laresapan,

national laraacepam shortage. We were just out like we didn't have any. And I started thinking about though and so many of our families were saying, hey, my kiddo is having breakthrough symptoms the next time their Ativan doses do. And I was like, well, I don't have any Atavans. And, but I can use Clonopin

and we can try to dose it three times a day. And so oftentimes I always start with Ataban because I mean, Atavans the gold standard for sure, right? Like, no one's contesting that. But if I have a family who says, hey, this is working great, but around noon when I'm supposed to give this next adivine dose, we're having a ton of mannerisms and stereotypes and self-injury,

I'll switch to clenazepam in that setting. And I have used ayazepam successfully, but I think its half-life is so long. I think it's more likely to cause sedation and stupor as a consequence of the as-a-a-a-a-a-a-a-cad-a-old. So, yes, generally I will consider longer-acting benz-a-a-pines of folks are having breakthrough symptoms, for sure.

Have you personally, in your clinical experience, seen Mementine give any significant benefit? that's a great question i had so other 45 kids that we treated in that study we had one kid who didn't need any benzos and i treated him with memantine and it was like gangbusters that's not i think the majority of cases and most of the time when i'm reaching for memantine i'm using it in conjunction with the benzo so i don't know if i can really give a lot of credence to just using memantine as monotherapy because oftentimes it's it's i'm using both of them at the same time got it okay so in kids without autism, what type of catatonic symptoms might be there that might not be in someone with autism? So there's not a specific symptom that I would expect to see in a neurotypical kid that I would

not expect to see in a neurodivergent kid. The symptoms are crossover significantly, but there are symptoms in kids that I would not expect to see in adults. And those are specific in the like the pediatric catatotinorating scale. So that includes acrosinosis, cold extremities. That's that's in the pediatric catatonia rating scale, but not in the Bush Francis. New onset urinary incontinence is also in the pediatric catatonia scale, but not in the Bush Francis. Schizophasia is similar as well, scrabled speech, and then automatic compulsive movements. So I think it's actually more of a delineation between adult catatonia and pediatric catatonia

relative to like neurotypical or neurodivergent catatonia. I think you can expect pediatric specific symptoms rather than, like, in adult-specific symptoms rather than neurodivergent or neurotypical specific symptoms. What about when you first start treatment with the Ativan Challenge? I think that I read somewhere and I can never, I couldn't find this article. I feel like if it exists, I may have read it five years ago, but I seem to have read somewhere that if you give an Ataband challenge, in some cases, the Bush-Franc score may go up, but it still can be confirmatory of the Catatonia diagnosis.

Does that sound familiar? Sure. Yeah, I think that I don't know if I've read that paper, but that is my experience where, particularly if a kid is stupress or like not engaged and then you treat them and they have hyperactive symptoms, you could definitely have an elevated Bush Francis, right? Like if a kid is stuporous and has waxy flexibility and you treat them and then they start, they're aggressive and impulsive, your score could go up. But in theory, that's a positive finding, right? So, you know, the Bush Francis is, I mean, it's revolutionized the way that we take care of. catatonic patients. But at the same time, it's not a, it's not a perfect assessment for looking for clinical improvement. And in fact, we, in our larger one study I referenced, the inpatient study with the 150 kids, we found statistically significant improvement in the Bush Francis for kids that were admitted and discharged. But we didn't find that the Bush Francis correlated with any other symptom severity metrics. So like length of hospitalization, dose of benzodiazepines, the score of the Bush Francis did not correlate with those sort of secondary,

clinical outcomes, right? But when we first looked at it, I thought a Bush Francis of 30 would be indicative of a longer length of hospitalization or a higher dose of benzos, but that wasn't the case. And so I think what that means is that we just need to consider the Bush Francis a tool for those assessments, but then also be aware that a score change on the Bush Francis is just another, you know, data point for you in your sort of overall clinical assessment. I would like to go through and do rapid fire like I'll say the the Bush Francis like the word that's associated with like the scoring and you tell me how it presents in someone who's a child and adolescent okay a child adolescent or a kiddo with autism you can differentiate it if you want okay okay okay

excitement so frenzied frenzied motor activity not being able to stop moving bouncing around the room despite having high doses of sedating medicines immobility stupor so immobility and stupor I think is is well described so essentially like limited movement limited engagement not interacting with the interviewer mutism again excellent description not not speaking or not well let me refrain a neurotypical kid who is usually verbal limited at verbal output or no verbal output neurodivergent kiddo who uses sign language or aAC device stopping you using communication devices. Staring. Staring is tougher. So it's well described, right, where it's like poor eye contact and limited eye contact.

The worst iteration of that is fixed gaze or not shifting attention across the room. But what I'll say is that you can also see that in discrete moments or periods, where it's like they're having a few seconds of staring. It doesn't have to be an hour-long experience. Posturing, catalypsy. again, holding abnormal odd movements for extended periods of time, but again, similar to the staring,

you can have that posturing, but it doesn't have to last an incredibly long amount of time. So particularly in our neurodivergent folks, what we've seen, is they'll have posturing the last seconds, but they'll be in the middle of an aggressive episode or hyperactivity, and they'll do this, and then they're back at it, right? So I think we have this sort of classic hypoactive version of catatonia in our brains a little bit, where it's like they have to be doing this for an hour, That's not necessarily the case. Grimising. Grimising is tough.

It's involuntary facial expression where you're doing gestures like this. And then you can have prolonged cramping where folks will hold that position for 10, 20 minutes longer for an hour. Echopraxia, echolalia. So echolalia and echopraxia are the mimicking of either movements or words.

right? So you say something back to them and they'll say it to you, say it to you, say it to you, say it to you. So that's echolalia. Echopraxia is the mimicking of movements. They're watching the examiner do. Right. Exactly. Yeah. So David's doing doing it, doing it. He's engaging in acropraxy now. What I will say is that you can see echolalia and acropraxia at baseline for autism, right? So it's really critical to talk to the family about was your kiddo having echolalia and acropraxia before they had the mental status change? And if they are, is this more frequent than what they had been doing, again, trying to establish a baseline and determine if it's a departure from it. Stereotypy. Stereotypy. So, again, the flapping. So this is an interesting distinction. So a lot of our trainees have a difficult time with delineating between stereotypes or mannerisms.

And the way that I conceptualize it is stereotypes are repeated movements, right? So like hand flapping where there's like a frequency to the movement, that's a stereotypity. And then the canter, not the Bush Francis, but the canter measures stereotypes in terms of self-injury. So if it's like head slapping, that would be a stereotypy resulting in self-entry. Does a stereotypity have to be different from a stem that's present at baseline? No. Mannerisms. So mannerisms are odd movements that seem to have no necessary purpose.

The classic example is someone randomly saluting, right? But again, in the canter, they judge that based on some. self-injury. So the higher, if self-injury is a part of that, it's a higher score. And that can include things like swallowing coins, guiding, like trying to stick a finger in the eye, so on and so forth. Annabow, why don't you ask a couple of these? Yeah, I'm not going to go quite as in order, but anyways, I want to know, how do you describe Mitt Gahan? Mickahen is this, it's the passive engagement with the examiner, right? So the classic example is you lightly tap on someone's arm and they drift all the way up, right? And then they hold it there.

So it's a, it's a passive, it's passively following a suggestion, right? So that, that's the sort of classic distinction of it, or the idea of conceptualization. Is, would it be positive, even if like the hand goes up a little bit? Yeah. Not necessarily doing the whole angle poised lamp. Okay. What about Gaggen-Halton? Gigan-Haldon is, is equal and opposite resistance when you're doing an exam. So the example I give is I always grab someone's arm and I measure their tone, right, because you can have increased or decreased muscle tone in the setting of catatone. The Bush Francis only measures increased. The canter measures both flexibility and rigidity. So I measure for that. And then I'll pull against their arm. And if I'm pulling and they're

giving me equal and opposite resistance when I am trying to extend their arm, that is what that's a positive sign for digging home. Got it. What about automatic obedience? Automatic obedience is, it's a tougher assessment. The canter actually combines impotendency in automatic obedience, but in theory, automatic obedience is following instructions after being asked not to do so. So the classic one is like, I have a needle in my pocket. If you stick out your tongue, I'm going to stab your tongue.

Don't stick out your tongue. Don't stick out your tongue. For kids and for folks that are neurodivergent, I just say, I'm going to ask you to shake my hand, don't shake my hand. and then I'll extend my hand and see if they shake it. And that way there's less sort of, that's my own practice, but that way there's less questions being asked of them or less commands they have to follow.

What about verbijuration? Forgeribration is basically nonsensical noise production. So if you watch the YouTube video, the boy on the YouTube, he screams at the floor. And that's what I would call virgineration. He had been verbal. So he went from verbal to nonverbal to screaming. So that sort of, and again, nonsensical noise production is however categorized riguration.

So rigidity? Did we do that one? Mm-hmm. Yeah, so increased or decreased muscle tone. Increased on the Bush Francis, increased or decreased on a canter. Negativism? So we talked a lot about oppositionality. That follows into that category of negativism. So is it oppositional because a kid is being oppositional, or is it negativism because they can't follow your instructions?

that's the delineating line there. Waxy flexibility. So that one is like if you put their arms in a position and they hold it like a candle, right? So that's more of the classic version of Catatonia. Like if you Google Catatonia, you'll see someone who has Waxy Flexibility. And essentially, like, you can put them in this position

and they'll hold it and they'll kind of slowly drift down over time. How's that different from passive obedience? I mean, you mean, from the Micahen? Yeah. So the Micahen, you're actively, you're doing something, right? So you're tapping their arm

and they're following your suggestion. That's Micahen. Waxy flexibility, you put their arms there and they hold it and then they slowly drift down over time. You could make the argument that they're two sides of the same coin, essentially, right?

Like there's this passivity of allowing you to put their limbs in different positions, but they're just two different ways of assessing that. I think about posturing, in catalepsy and that feels pretty similar as well. Yeah, it's, it's that you're essentially assessing similar symptoms in different ways. Got it. Withdraw. So withdrawal is primarily

categorized as food, liquid or food intake onto Bush Francis. Impulsivity. So again, impulsivity is pretty, I think pretty descriptive. But what I would say is that in catatonia, of that can become so severe that it's life-threatening, right? Where people are jumping off of, you know, a second-story balcony, or they're swallowing coins, or you're running into the streets spontaneously. So it can have a very severe overall presentation. Automatic obedience? I think we talked about that one.

Yeah. Yeah, we did automatic obedience make game game. Did we do Ambit Tendency? No, but Ambitendency is fascinating. So ambit tendency is essentially getting stuck in a movement or stuck in an action. So if you ask someone to shake their hand and they reach out and they get stuck from actually doing it or they're reaching for a cup and they can't completely, like cannot completely initially finish picking up the cup. And another example of that is actually when people cross different floors. So if you have tile floor to carpet floor and they can't walk across that or they can't walk through a door threshold, you can see that as well.

How about grass reflex? Grass reflex is just folks they're grabbing everything is next to them. It's not the neonatal sign where you rub the inside of the hand. It's essentially like grabbing everything that's next to them. Perseveration.

This one is very, very tricky to delineate in autism because the core feature of autism, criterion B, is restricted interest repetitive behaviors, right? So is this restricted interest repetitive behaviors or is this perseveration. The way that I, so perseveration is like an obsession with what's happening or a movement,

a physical movement that won't stop. So someone's like moving their hand like this and then they can't stop moving their hand, right? Then how do you delineate it if it's a cognitive perseveration? So we've had folks in clinic who, for example, they love, you know, they love cartoons, right? So they want to watch cartoons all the time. And that's when they're autistic without having catatonia, then they develop catatonia and they only want to watch the same three seconds of the same show forever. So that's the distinction, right? It's an increased level of severity and frequency rather than the like restricted interest repetitive behavior. Then combativeness. We talked about this, but go ahead. Yeah. I mean, again, it's the,

it's the frequency, severity and nature of it. Can you go outside without your, you know, patient attacking somebody, right? And it is indiscriminate and without having a, you know, a reason for, the aggression occurring or, you know, they're not, it's not that they're scared or they're not trying to, or they're trying to communicate. It is an indiscriminate sort of aggression. Automatic or autonomic abnormality.

So this is a really interesting one that we've discussed a lot institutionally, because so we were at that paper and we developed a roadmap for assessing these kids, and it's how do you define autonomic instability in a kid who's catatonic? And so essentially what I would say, if their heart rate is elevated,

their blood pressure is elevated or opposite, if it's too low, then those can be considered autonomic instabilities, but those numbers are not hard and fast. I think it's, again, tracking over time what those look like. Okay.

This is great. This is really good. Yeah, thanks to the invitation. This is so fun, and I've learned so much. Thanks. Yeah, why I really appreciate you guys being willing to have me on. It was at a great time.

Thank you. This was probably the most fun I've had today. Oh, great. Oh, so good. Great. Well, okay, so like, we're, just for the audience, like, let's say someone was listening to this and they're like, how do I get help in my state where I'm living? Like, is that even available?

What would you say? So there's the catatoniafoundation.org. They're a nonprofit who, or their whole mission is to try to plug people into resources. So I would start there. Folks can email me if they really need to. But I think just trying to, you know, touch base with organizations like the Catatonia Foundation is where I would start. Okay. And your

clinic name is? It's the MIN clinic. It's medical exploration for neurodevelopmental disorders. Okay. Well, this is wonderful. I know you said an hour I like to be timely. So thank you so much. Of course, thank you so much.

Yeah. Keep me posted if new developments happen or if you feel like there's a talk or someone that I should consider having on, I would love to hear. You're kind of in that world more than I am, but I'm definitely passionate to educate people. Sounds great. Thank you, guys. All right.

Thank you. Thank you.