Dr. Daniel Knoepflmacher (Host): Welcome to On the Mind, the official podcast of the Weill Cornell Medicine Department of Psychiatry. I'm your host, Dr. Daniel Knoepflmacher. In each episode, I speak with experts in various aspects of psychiatry, psychotherapy, research, and other important topics on the mind.

Our topic today is catatonia, a neuropsychiatric condition that arises from a range of psychiatric illnesses and other medical conditions. While it's more commonly identified with slowed or absent physical movements, delayed speech or mutism, and other characteristic physical exam findings, catatonia can also present with agitation marked by excessive hyperactive, typically purposeless physical activity.

Catatonia is a fairly common finding in inpatient psychiatry with a reported prevalence estimated to be about 10% of patients in these hospital settings. If left untreated, it can lead to significant medical complications and mortality. Malignant catatonia is a life-threatening variant that includes instability in the autonomic nervous system with major swings in blood pressure and heart rate, significantly elevated body temperatures, and other critical symptoms.

Without prompt treatment, it has an estimated 50% mortality rate. Since many of you listening may not have directly encountered catatonia before, I'll share my first clinical experience treating a catatonic patient who I met early on in my training. She was 20 years old at the time and in her third trimester of pregnancy. She'd been hospitalized psychiatrically several weeks before for a manic episode, which was the first she'd ever experienced. During her hospitalization, she developed catatonia and had just been transferred to our unit for more intensive medical care.

In our first meeting, I found her sitting upright in bed, statue-like, speechless, staring blankly at a wall. She was unable to blink, leaving her eyes red, swollen, and dry. She exhibited several of the other telltale signs of catatonia, which we'll talk more about later in this episode.

And when I gently lifted her arm, it remained suspended in the air. Her inability to eat or drink were making things increasingly medically tenuous for her and her baby. Soon after we evaluated her, she was given the medication Ativan through an IV. And within several minutes, her frozen state began melting away. She was able to move slowly, as if moving through invisible molasses, and began eating soup and drinking juice. We arranged for electroconvulsive therapy or ECT to start the next day. By the following week, I saw her walking through the unit, talking and joking with her family. She went on to give birth to a healthy baby at full term and later became my patient in the outpatient clinic.

Today, the residents in our training program all gain extensive experience diagnosing and treating catatonia, something I get to witness when I round with them on call in the hospital. They all have much more experience and mentorship in the assessment and treatment of catatonia than I had as a resident. And one of the key people responsible for this change is joining me today, Dr. Leonardo Lopez, who is the Vice Chair of Inpatient Services here at Weill Cornell Medicine. He's a prior guest on the podcast who came on before to speak about schizophrenia, and that's an episode I highly recommend if you haven't already listened to it. Leo, it's great to have you back.

Dr. Leonardo Lopez: It's a pleasure to be here, an honor to be here. This podcast has gotten quite a bit of acclaim, and I think a much larger listener base since the last time I was on, but deservedly so. So, I'm really thrilled to be here to talk about this topic.

Dr. Daniel Knoepflmacher: Well, it's with guests like you that that happens, obviously. So, want to ask you how you actually developed an interest and so much expertise in catatonia.

Dr. Leonardo Lopez: Yeah. So, I would say, at this point in my career, catatonia is certainly my guiding clinical and academic interest. It wasn't always that way. as you sort of alluded to before, I started my career primarily interested in schizophrenia, particularly in treatment-resistant schizophrenia, where patients don't respond to conventional antipsychotics.

Often you have to treat them with clozapine, which we talked about on that podcast. And when clozapine fails, often you will augment it with ECT, which you mentioned during your introduction. So, as a consequence of that interest, I started to get interested in ECT and learned how to do ECT and began to perform ECT clinically. And when I started to do ECT clinically on a regular basis, I noticed that there was a great deal of catatonia that was being missed by the doctors that were sending their patients to ECT.

And there's a really interesting way, I think that you can notice this if you're an ECT doctor, and you also alluded to it in your introduction. When, you bring a patient down for ECT, they have to be hooked up to monitors, right? To monitor their heart rate and their oxygen saturation, their blood pressure, and so forth. And I would see anesthesiologists lift up the patient's arms to wrap the cuff around their arm and then let go, as one does, and see their arm remain suspended in the air. And I saw this happen over and over again and, you know, I would call the providers and say, "Did you realize that your patient was catatonic?" They'd say, "No, the patient was depressed. We're sending them for depression," or, "The patient has schizophrenia. We're sending them for that reason." and in fact, I said, "Well, you know, well, you should start the patient on some Ativan, and good news is they're getting ECT. It's the right treatment." But I became fascinated by how much catatonia was being missed, and so I started to spend a lot more time with my services.

I, eventually, was in a position to be able to run inpatient services. So, I started to spend a lot more time with my services, systematically trying to evaluate and diagnose catatonia, trying to make sure that everyone had it in the forefront of their mind diagnostically. And, as time went by, that just sort of snowballed and became the centerpiece of, what I do.

Dr. Daniel Knoepflmacher: just love that story of the regular part of an exam for an anesthesiologist and seeing the patient's arm remain suspended, because it touches on empirical thinking, right? You were there and you were watching and saw an empirical finding that then led you to say, "Gosh, there's a lot of untreated catatonia out there."

And it reminds me of how a lot of these diagnoses were first categorized by often in Northern Europe, some German, Swiss, you know, psychiatrists. And we talked about that actually a lot when we talked about schizophrenia. And there's a link here between schizophrenia and catatonia, which maybe is a little overvalued in some ways originally.

But anyway, I want to get into the history and go back to some of those original people who observed this. in 1874, Dr. Karl Ludwig Kahlbaum identified this as a distinct clinical entity, and he actually described a lot of the core features we observe today. He even to this point about linking it to schizophrenia, he didn't link it just to schizophrenia and felt that and observed that it arose in different illnesses.

And then, Kraepelin and Bleuler, who were very important in schizophrenia, and who we discussed in that episode, they tied it more to schizophrenia, which certainly there is a linkage there. And that notion, as I understand it, was persistent well into the 20th century. If you look at, I think, DSM-I through III, they talk about schizophrenia with catatonia.

But things have developed since DSM-III. So, I'm just curious if you could give us a better history than I just did of the conception of catatonia and how that has grown and developed into what our current understanding is today.

Dr. Leonardo Lopez: Absolutely. So, am I allowed to start in the 19th Century?

Dr. Daniel Knoepflmacher: Yes. course Whatever you like.

Dr. Leonardo Lopez: Okay, great. Yeah. So, Kahlbaum was the first person in the medical literature to utilize the term catatonia. Some would argue that the first description of catatonia in the literature generally was not due to Kahlbaum, but was due to Herman Melville, and specifically his short story "Bartleby, the Scrivener," which I highly recommend everyone read. It doesn't take that long. And it's a story about a clerk who's hired by a Wall Street attorney and, gradually becomes sort of contrary, has prolonged periods where he doesn't speak and stares at walls, withdraws increasingly from work and society, and ultimately stops eating and suffers from starvation. There are many people who read that and read catatonia in it. There are alternate readings as well. But it's always valuable, I think, to go to the true literature, and read descriptions of what we see in the clinical realm.

Kahlbaum's term, catatonia, which I think is arguably the longest, term in continuous utilization in the psychiatric literature. He did coin in a manuscript that he published in 1874. The term, taken back to Greek roots, means something like complete tension or tension all the way down.

The manuscript actually utilizes a second term. One is catatonia, and the second is Spannungsirresein, apologies to our German listeners, which translates as tension madness. I think that's a great way to conceptualize catatonia, and we'll talk about it a little more later.

Kraepelin took it up when he was developing his concept of dementia praecox, and he referred to catatonia, which he initially did believe was a quote, "peculiar form of dementia praecox." He referred to it as paralysis of the will. And, as we go through this, I imagine I'm going to talk about that concept a lot, because I think it's central to the idea of catatonia.

But he did believe it, at least in his early writings, to be part and parcel of schizophrenia. And Bleuler, who disagreed with Kraepelin about a large number of things, agreed with him on this point. Both of them, towards the end of their career, sort of suggest in their writings that perhaps that view is incomplete and that catatonia can occur in other mental conditions as well.

But those writings are sort of overpowered by the earlier writings. And as you pointed out, many, many years, catatonia was considered to be a manifestation of schizophrenia and schizophrenia only. The words catatonia and catatonic, in the first three editions of the DSM, which were published, in 1952, '68, and '80, all of them manifest the word catatonia only in association with schizophrenia and related disorders.

So, all the way out to 1980, you're really not seeing literature that suggests—you're not seeing in the DSM anyway—a suggestion that catatonia can exist outside of schizophrenia. It was work in the mid-70s by Max Fink and Michael Alan Taylor that started to undo this narrative. They published a paper in 1976 where they looked at patients with catatonia in two New York area hospitals and found in their sample that the overwhelming majority of the patients had bipolar disorder.

And in fact, subsequent literature by their group and related groups suggested that bipolar disorder and unipolar depression were both major causes of catatonia. So, when the DSM-IV is published in 1994, you still see a deep connection between schizophrenia and catatonia. However, the mood disorders can now be qualified as having catatonic features, and there is also a diagnosis of catatonia due to a general medical condition. Between the 1990s and the 2010s, I think we learned a lot, which we'll get to as we go through this today.

And finally, in DSM-5, we got a list of nosologic criteria for catatonia for the first time. I should say that in previous editions of the DSM, catatonia was almost always described circularly. For example, the DSM-3 will say that you can say that someone has catatonic schizophrenia if they display symptoms like catatonic mutism or catatonic stupor without explaining what is catatonic about the mutism or the stupor. It wasn't until DSM-5 that we got true, sort of standard nosological criteria. So, a bit of an irony there, right? That it's the longest term in continuous use, and yet it was 140 years before we got clearly defined criteria.

Dr. Daniel Knoepflmacher: That's a good segue into what catatonia is and what it looks like. Talking about the nosology or what are those characteristic symptoms and signs. So, can you tell people who, you know, have never seen it before or experienced what this looks like clinically what you see when you're examining someone for catatonia?

Dr. Leonardo Lopez: So, I will go through the criteria, but I like the way you phrased that question. Tell them what I see, because before I get into the criteria, I would like to put a little bit more of a conceptual frame on catatonia rather than just listing symptoms, which is what you see in the DSM.

It's important to know the list of symptoms, but it is also important to have a broader concept of what's going on in catatonia. And that brings me back to Kraepelin's term, paralysis of the will. I would conceptualize catatonia as a disruption in a person's ability to turn their will into action or to achieve a goal through their will.

So if you'll allow me to use an example of this, right? So, let's say you're at dinner and you sample your, dish and it's insufficiently salty. So, you think to yourself, "I need to get the salt," right? So, there are two ways that you might do this. One is that you will reach across the table, put the salt shaker in your hand, and bring it over to your plate and put the salt in. So, what have you done there? Well, your will has translated itself into action through a motor behavior. Your will has translated itself into action through a motor behavior and allowed you to achieve your goal. That's one way you can do it.

The second way you can do it is you can look across the table at the person sitting across from you, assuming you're not eating alone, and you can say, "Can you please pass me the salt shaker?" And then, they will pass it to you. And in this case, your will has been translated into action through a speech behavior, right? And you've achieved your goal. So, there are two ways to turn your will into action. One is through motor behaviors, and one is through speech behaviors. Catatonia is a condition where your ability to do that translation from will to action through motor behaviors and speech behaviors is disrupted, but it can be disrupted in all sorts of ways, which we can talk about in more detail when I go through the criteria. But if you just think about it conceptually, how might your ability to turn your speech into action fail? Well, the simplest way is you can no longer speak, right?

How might your ability to turn your motor behavior into action fail? Well, the simplest way is that you can no longer move. But there are other ways, right? For example, perhaps you can initiate a movement, but then you get stuck initiating the movement. Or perhaps you initiate the movement and then retract it, and then initiate it again and retract it, and you get stuck in a repetitive cycle. Perhaps you outsource your motor behaviors to other people, allowing them to move you themselves, right? Rather than moving on your own. Or imitating their movements, right? Rather than willing your own movements. Or perhaps you simply stop moving entirely. And speech works very similarly. Perhaps you initiate speech but get stuck and repeat the same phrase over and over again. Or perhaps you outsource your speech to another person and wait for them to talk, right? And then, imitate what they say. Or perhaps you stop speaking at all. There's all sorts of ways that your ability to accomplish something with movement or speech can get disrupted, and all of those are present in the psychomotor syndrome we call catatonia.

So, perhaps this now is an opportunity to go through the list of criteria so that people understand them. So, there's 12 criteria, of which you have to have three to meet the DSM standard, and you can group them in all sorts of ways. I, tend to group them one of four ways. So there are three criteria that have to do with the way you interact with the world or the environment, and those are mutism, meaning, no speech or very limited speech or soft incomprehensible speech; stupor, meaning that you do not interact with the environment from a motoric point of view. So for example, you know, you don't utilize tools like a fork and knife; and ,therefore you don't eat, right? When people walk into the room, you don't follow them around with your eyes. You simply stare straight ahead. And negativism, which means, broadly speaking, being contrary or doing the opposite of what you're told. The classic test for this is to extend your hand to a patient and say, "Do not shake my hand," and then watch them lift their hand and shake it. And then, you put it back down and you say, "Please pay close attention. Do not shake my hand," and their hand pops up and shakes it.

Then, there are a group of symptoms that have to do with positioning, and you referenced several of these in your introduction. So, one of them is called posturing, which means that the person maintains an unusual or uncomfortable posture, in opposition to gravity, right? So, they will stand on one foot for a long period of time, or they'll stand in the sort of Karate Kid position for our listeners who are old enough to know that reference or similar things for a period of time.

Then, there is catalepsy, which is a similar concept to posturing, but means that you have been placed into the position by the examiner. You described, right, lifting the patient's arm. I described it with the blood pressure. This is called catalepsy. Waxy flexibility, which is the sensation you get when you move a patient from one cataleptic position to another. And despite, the many, many written descriptions of this sensation that I have read, I've never found one that is sufficient. You simply have to experience it, and feel it to know what it is. I just don't think there are words that do it justice. And grimacing, which is maintaining odd or unusual facial expressions for extended periods of time.

Then, there's a group that have to do with repetitive movements, and I talked about repetitive movements a minute ago. Those are called mannerisms and stereotypies. Mannerisms are repeated movements that are clearly not goal-directed. They are odd or unusual. And stereotypies are movements that are not odd or unusual and appear goal-directed at first, but then they are repeated so many times that they're clearly not in the service of any such goal.

So, I saw a woman recently on our inpatient unit who was sort of scratching the back of her head and then would put her arm down and would scratch it again, and then would do it and would scratch it again, and did this continuously probably for eight to 10 minutes, which is an example of a stereotypy, right? When you first see it, you think to yourself, "Okay, the back of her head itches. That's fine." But then, as you see it happen over and over according to the same rhythm, you start to think there's something unusual about this.

And then, the last group are what are called echophenomenon, echopraxia and echolalia, meaning that you're imitating behaviors that you see in front of you. So echopraxia means that you are see- imitating the movements of the person directly in front of you, and echolalia means that you're imitating the speech of the person in front of you. That's 11.

The final category is agitation, and you referenced this earlier. And I think this is one that causes a lot of confusion, both because people traditionally think of catatonia as being people who are mute and frozen. And because agitation is often conceptualized by both psychiatrists and non-psychiatrists as instrumental in some way, right? Like, the person is agitated because of something, and they are trying to achieve something through their agitation, right? They're yelling, they're screaming because they're angry or they need to express themselves. They want to get something out of it.

The agitation in catatonia that you referred to is not like that at all. It's completely purposeless, and not directed towards any meaningful goal. So, you'll often see patients with catatonia, for example, do somersaults or cartwheels through the hallway, and be in continuous motion doing so. I recall a patient I had once that would sort of put out his arms like an airplane and just fly around my unit and run into walls. This is the kind of agitation that you see with catatonia. The person is not trying to achieve anything because, of course, as I said before, they're not capable of translating their motor behavior into something that can achieve a goal.

So, that's a broad overview. You need three of those 12, of which there are many, many combinations possible, right? So, the trick with diagnosing catatonia is that you have to be aware of all of these symptoms and the way they interact with each other and look together. It's not enough to simply say, "Well, the person is not talking, therefore they're catatonic," or, "The person is talking again, therefore they're not catatonic anymore."

Dr. Daniel Knoepflmacher: That's was a beautiful review of what catatonia looks like, and I love your conceptual framework for it. It touches on something, which is that tension, that underlying tension. I actually think when I talk to people who ask about catatonia and are unfamiliar, they assume that this is an a state of hypoactivity, of an absence of excitation or something going on.

But what you're alluding to in the tension is that this is a situation where there's excitation going on neurologically, neurobiologically. So, what have you learned from patients in talking to patients about the experience of what's underlying? And we'll get to the neurobiology in a moment, but I'm talking more about what it's like for them to be catatonic.

Dr. Leonardo Lopez: This is a very difficult question to answer. And just like the presentations in catatonia are heterogeneous, the answers you receive from patients to these questions are also heterogeneous. There are definitely patients who have a clear recollection of the experience and can tell you, "I couldn't move and I couldn't speak."

There are other patients who don't have that clear recollection of the experience, but they can tell you that they experienced something. Usually, it's that they were frightened, or fearful and were uncertain about what they were supposed to be doing. And then, of course, there are patients who have no recollection of the condition whatsoever.

There's not great literature on this. There was a paper out of a group from South Africa in 2022 that sort of tried to look at patients' subjective experience of catatonia, and they looked at 40 some odd patients and found that somewhere between a third and half the patients could describe experiencing the symptoms that were perceived by the examiner, right?

So, something like 30% of patients who were found to be mute could say, "I recall being a period where I was mute," right? Or, approximately 50% of patients who were described as sort of frozen in place could say to the examiner, "Four to eight weeks later, "I remember a period where I was frozen in place."

But the rest of the patients, either gave a more subjective response, often related to fear or uncertainty, or simply were not able to relay any experience. I think what we try to tell trainees when you're in the room with a catatonic patient is because we have this uncertainty about what the experience is like, both in general and on the individual patient level, you always need to behave as if the person is hearing everything you say and reacting to it.

So, the fact that the person is mute and not interacting with you should not mean that you don't interact with them like they're a patient in a room who can hear and understand you. Whether they are or not in that moment, impossible to say, on a patient-to-patient basis, but it's possible. And so, everyone should treat the patient as if that were the case.

Dr. Daniel Knoepflmacher: And that reminds me a lot of anecdotally my experience with mania in talking to people's recollection of the experience of mania, which some people, as if they were blacked out that whole period and others can talk with much more detail, which is another state of excitation. So, can you talk about what we know about the underlying neurobiological process that is creating this condition?

Dr. Leonardo Lopez: I think I should start by saying that I think we know very little, which is not to say we know nothing. We do know some things, and I'll get through them. But there's a fundamental problem in studying this condition, right? Which is any human subjects research on patients with this condition that involves really investigating the neurobiology is going to involve obtaining their informed consent in some way, and yet there's a very, very, very large proportion of catatonia patients who simply cannot provide informed consent either, because they cannot interact with the examiner or investigator at all or because they have something that we'll, get to later, I think, called automatic obedience, where in fact they do exactly what they're told, no matter how unpleasant to them. So, it's a very difficult thing to study.

That said, we do have some literature on the underlying mechanisms of catatonia, primarily drawn from the population of patients with catatonia secondary to schizophrenia. We have, I think, the most convincing and replicated evidence is fMRI data that shows hyperconnectivity between the supplementary motor area, the pre-supplementary motor area, supplementary motor area, and the motor cortex.

So, these are brain structures, the SMA, and the pre-SMA, that are involved in selection, initiation, inhibition, and timing of movements. And they translate that sort of motor planning into motor action. So, we know pretty convincingly that there is aberrant connectivity between these regions in catatonia patients, which gets back to my paralysis of mine—Kraepelin's, I took credit for it—but Kraepelin's paralysis of will concept from before, right? Where there's this idea that you have this ability to plan or initiate action, and then you have the actual action, and you cannot turn one into the other. So, that I think is the piece that's most clearly studied and documented.

There's also evidence, for example, that the orbitofrontal cortex ihas aberrant connectivity with the premotor cortex. There's evidence that disruptions in GABA transmission have something to do with catatonia, which will not be surprising to people when we get to treatments later. For example, there are SPECT studies that show reduced GABA A receptor density in the somatosensory cortex.

So, there are a variety of brain regions implicated. I think the most strongly implicated are the supplementary motor area and the M1 motor cortex. I will say, however, that, like I said before, this is all drawn or almost entirely drawn from schizophrenia populations. And catatonia is a transdiagnostic entity. So, there's no a priori reason that the mechanism of catatonia should be the same in one condition and in the next.

It may be something more like hyperthermia, right, which is an indicator of illness and it's usually an indicator of an infectious illness, but not always, right? And it's usually because of prostaglandin synthesis in the hypothalamus, but not always. There are other explanations, too. Catatonia may be something more like that. We don't know enough to say. But I'm encouraged that what we do know fits neurobiologically with what we see and understand conceptually that I described before.

Dr. Daniel Knoepflmacher: What about diagnosing? I mean, you went through criteria from the DSM, and you talked about this conceptual framework. How do we best diagnose catatonia?

Dr. Leonardo Lopez: I think we best diagnose catatonia the way we best diagnose everything in psychiatry, which is listening, observing, and talking to the patient, and also putting our hands on the patient. This is a crucial part of the catatonia diagnostic process that is often neglected by psychiatrists for a variety of historical professional reasons, right?

But I think it starts with observation. Sometimes it is easy to observe, right? The patient is completely mute and not interacting with their environment. It's not difficult. But sometimes it's more subtle than that. And I think, from my own point of view, what I tend to look for first is repetitive movement. Repetitive movements are not specific to catatonia, right? We'll talk about sensitivity and specificity of these findings perhaps later, but they are frequent in catatonia, both stereotypies and mannerisms.

So typically, when there's some suspicion that the patient has catatonia, I will start by looking for those things. Looking at their fingers, looking at their toes or their socks, trying to see if I see some sort of behavior that's happening in a repetitive fashion that I can't explain. If I see something like that, the thing I often do next is do, on my own, while I'm speaking to the patient normally, some sort of exaggerated movement.

For example, because we're not on video, but rubbing the top of my head or doing something strange with my arms to see if they'll imitate me. Because echopraxia is extremely specific, unlike the other symptoms I just mentioned, very unlikely to be seen in conditions other than catatonia. And if I can draw that out quickly, then I know the patient is probably catatonic.

And then, I would say the last thing that I always do is examine their arms, like you said before, and try to see, if when I position them against gravity, if they remain in that position. Again, like echopraxia, essentially no explanation for catalepsy other than catatonia.

So, those are the key things. But I think most important thing, like I said before, it has to be in the front of your mind. And it should always be in the front of your mind if you're on a psychiatric unit. You mentioned before that the data suggests that 10% of patients on psychiatric units have catatonia. I think that data is correct. It should always be in the front of your mind, and you should always have your eyes on it, right? You shouldn't wait for it to come to you, right? If the person is mute and not moving, it's come to you, and you haven't really done any work. You have to search for it. And I think, my own practice, I think repetitive movements are often where I search first.

Dr. Daniel Knoepflmacher: The Bush-Francis Catatonia Rating Scale, which is well-known as an instrument for assessing for catatonia, encompasses a lot of what you've described. Is there anything else specific, you know, about the Bush-Francis Catatonia Rating Scale that you think is important to

highlight?

Dr. Leonardo Lopez: yes, several things. so the Busch-Francis Catatonia Rating Scale, which was developed in 1996 by, George Busch, not that one, or the other one, I guess, Andrew Francis and George Petrides. that scale was developed before development of the DSM criteria. So at the time, it was developed both as a diagnostic instrument and as a severity measure.

the diagnostic piece has been superseded by DSM criteria, which are more specific. In fact, there was a study that came out, I think in 2013, that showed that, people who met diagnostic criteria for catatonia on the Bush-Francis, only 73% of those met DSM criteria for catatonia. In other words, the Bush-Francis criteria, which is, perhaps without getting into too much detail, you have to have two criteria out of the first 14 questions.

those were much less specific than the DSM criteria. So, I think the first thing I, I would say is important is it... You should not be using it as a diagnostic tool. you should examine patients according to the symptoms that one draws out with a Bush-Francis, but you need to establish that the person has three DSM criteria to say they're catatonic.

Once you've done that, then by all means, do your Bush-Francis and you'll get some sort of score and, as it is a pretty good tool for assessing how severe catatonia is. We don't have really clear agreed-upon measures for what kind of score is moderate and what is severe and what is very severe.

And in fact, there are a few little tricky pieces to it. For example, you know, a Patient who's mute and very stuporous, can't do many of the other catatonia symptoms because they can't interact with you, right? So, like if a person cannot fix their gaze on you, cannot exhibit echopraxia. And if they cannot speak, then they cannot exhibit echolalia, right? And what you'll see sometimes when you start to treat catatonia is that the stupor will lift and some of the other catatonic symptoms will then emerge. So actually, it's not uncommon early in the treatment of catatonia for the Bush-Francis score to rise, even though the person is getting better, and then to come down.

So, it's not perfect, but definitely a useful instrument. It also features a variety of criteria that are not in the DSM, but nonetheless I think everyone in the field agrees are commonly seen in catatonia and can be useful clues for the diagnosis, if you're not sure. One of them, for example, is called ambitendency, where the person gets stuck between two movements, right? So, if you see a patient, for example, walking in their room and then coming out of their room, and then walking back in the room and then coming out of their room again, and you see this repeated a few times.

If you've just walked onto the unit and seen that, you should think to yourself, "Well, that patient's catatonic," right? So, the Bush-Francis introduces some concepts that are not present in the DSM that can help you, that can help lead you to the diagnosis. But mostly, I think now we use it as a severity measure and as a way to determine over time whether patients are improving or not improving with treatment.

Dr. Daniel Knoepflmacher: So for those of you who are not psychiatrists or those who are budding psychiatrists, there's lots of YouTube videos out there on people using the Bush-Francis Catatonia Rating Scale. And there's also some amazing German words that are used in it. Like, can you just tell people for instance what gegenhalten is?

Dr. Leonardo Lopez: Gegenhalten means essentially that the person resists your movement of their arm, and the more you try to move, the harder they resist, if that makes sense. So, as a general rule, neurologic rigidity is not dependent on the strength of the examiner's stimulus. Like, the person who's rigid from Parkinson's disease is just as rigid if you pull hard as if you pull soft. That's not the case with gegenhalten.

The other sort of central German term on the Busch-Francis is mitgehen, which means going with. And essentially, that is when you sort of just lightly tap the underside of someone's hand and say, "Please don't let me move your arm," and then push up, and they will resist not at all and move the arm wherever you move it around. People sort of describe it sometimes like one of those desk lamps that you can bend at will with very little effort.

So yes, there's lots of fun historical stuff buried in the Busch-Francis. And it's a useful severity measure, and it gives you clues to the diagnosis overall. Something all the training psychiatrists should learn how to utilize. But I would encourage them nonetheless to know the DSM criteria first and to be certain that they know the patient has catatonia before utilizing it, because there are a lot of cases where patients score on the Busch-Francis and yet don't meet criteria for catatonia.

Dr. Daniel Knoepflmacher: And you've given some great examples of things to look for. It's often missed, as you experienced when you were noticing treatment for schizophrenia with ECT, that there are patients that weren't identified as having catatonia. I did an episode of this podcast with Jeff Ha about delirium, and one thing we talked about was how often hypoactive delirium is missed. I think there's also an area of potential overlap here, and distinction that has to be made sometimes with hypoactive delirium and catatonia. Yeah, you've identified a few things, but I'm just curious, for somebody who's trying to distinguish between these two conditions, what would you advise them to look out for?

Dr. Leonardo Lopez: So, this is a complicated question. I think the first thing I would say is I'm not convinced that it's always the case that it's necessary to distinguish between the two conditions. The DSM is written in such a way that it disallows the simultaneous presence of catatonia and delirium by definition.

I would be interested to hear what Jeff has to say on this, but that's virtually no one's experience who spends a lot of time with catatonia. That in fact, we see a lot of overlap. And it's not just experience that suggests that. There was a really interesting study in 2017 out of Vanderbilt that was published in Critical Care Medicine, where they looked at something like 130 consecutive patients in the ICU who were either on vasopressors or intubated. And they administered the CAM-ICU as a delirium scale, and then they performed a Bush-Francis modified for the DSM-5 to see if the patients, one, were positive for delirium and, two, were positive for catatonia.

And what they found in this ICU was that unsurprisingly in this population, about three-quarters of them were delirious. But more interestingly, 30% of the patients had catatonia. And in fact, 35% of the patients met criteria for both catatonia and for delirium. Now, some of those patients are probably patients who genuinely had both. Some of them may simply be purely catatonic patients that the CAM-ICU is insufficiently specific to pick up.

But suffice it to say, I do think they co-occur, and I do think that there's hypoactive delirium. There's catatonia that is misidentified as hypoactive delirium not infrequently. So, I would suggest that any patient that you see that you suspect has hypoactive delirium, you do a full examination to draw out catatonia, the elements of catatonia to see if the patient is catatonic. And there major treatment implications to this, right? Which is why this is such an important question.

Dr. Daniel Knoepflmacher: Exactly. I mean, I think, this is a really great point you're making is there's a Venn diagram that's overlapping here, and hypoactive delirium, the treatment for that is to look at the underlying causes and alleviate those. But if you do that and there's catatonia, you're not addressing the catatonia necessarily.

Dr. Leonardo Lopez: That's right

Dr. Daniel Knoepflmacher: So, a really important distinction. We could probably keep going, but there are so many other things to talk about because I want to actually get to the etiology, and specifically what are the psychiatric and medical conditions that can lead to catatonia.

Dr. Leonardo Lopez: Yeah. So catatonia, and I didn't mention this at the beginning, but I think one of the reasons that, I spend so much time with catatonia and find it so interesting is that it is, to your Venn diagram point, sort of the confluence of the psychiatric and the medical, right? Both in the sense that there's this obvious mind-body piece to it, right?

There are difficulties, there are neurobiologic difficulties initiating action. But at the same time, there's this sort of more metaphysical idea about not being able to utilize your will. And because it's a syndrome that is so commonly seen in both conditions that are classically considered psychiatric and conditions that are classically considered medical, and it really blurs the lines between, you know, why exactly is it that we call something psychiatric and that we call something medical?

So, without getting too much into detail there, I'll say that the first thing to know about etiologies of catatonia, is what is commonly referred to as the 80/20 rule, which is that 80% of catatonia patients are catatonic secondary to a psychiatric illness, and 20% of them are catatonic secondary to a "medical" illness. This is a well-replicated finding. It's been replicated in both adult and pediatric populations. And I think is generally agreed upon.

The psychiatric conditions that are most associated with catatonia are schizophrenia bipolar disorder, specifically bipolar I disorder, and unipolar depression, often psychotic depression. Which one catatonia appears more in and which it appears less in is a matter still of debate after many decades of investigating this. I think my best read of the literature is that they're about split even. Perhaps it's a little more common in affective disorders, or perhaps it is seen more commonly in patients with affective disorders simply because affective disorders are more common than schizophrenia. But suffice it to say, seeing a patient with catatonia does not in and of itself help you understand whether the patient has schizophrenia or an affective disorder. They're very common in both.

That encompasses virtually everything that is unambiguously historically a psychiatric diagnosis. Then, there's this sort of middle ground, which typically gets grouped in the 20% range. Those are patients with autism spectrum disorder or other neurodevelopmental disorders, often with known genetic syndromes. For example, Phelan-McDermid syndrome is a common syndrome associated with autism and also with catatonia. And then, neurodegenerative diseases like frontotemporal dementia or dementia with Lewy bodies. Those are also conditions where we see in catatonia.

And then, the last group is the group that at least now would be considered unambiguously medical. And those essentially comprise autoimmune diseases, which we can get to more if we have time, and, epilepsy, either interictal or postictal catatonic behavior. There are a few others. There are sort of rare genetic inborn errors of metabolism that can cause catatonia in children. Those are usually known about in advance of the patient becoming catatonic. There are reports of patients with metastatic lung cancer who have catatonia. But for the most part, they divide into these sort of three categories: 80% schizophrenia, bipolar disorder, major depression, and then 20%, some combination depending on the age range of autism, neurodegenerative disease, autoimmune disease, and epilepsy.

Dr. Daniel Knoepflmacher: So, given that psychiatric diagnoses like schizophrenia, bipolar disorder, they don't develop in children typically in the typical course. And then, something like a neurodevelopmental disorder, other medical things might be more a bigger percentage of the population at different age groups.

Like, we're not having Lewy body dementia in many 20-year-olds. So, there's a real variety across the lifespan, it sounds like. And you alluded to the pediatric cases. Can you say more about that specifically?

Dr. Leonardo Lopez: Yeah, absolutely. So, you're right. it's definitely the case that the age of presentation gives you some clue as to what the underlying cause might be. And the first clue again is this 80/20 rule, right? If you see a catatonic patient, four out of five chance it's a psychiatric illness. But age can help you as well. For example, like you say, if you see a five-year-old who's catatonic, it's extremely unlikely that that patient has schizophrenia, right? Now, there's a historical issue here, which is that because schizophrenia and then later bipolar disorder where sort of the diagnostic home of catatonia for many decades, most attention in catatonia went towards adults, right?

And there was a lack of recognition in catatonia in pediatric patients, because no one was looking for it, because why would you look for something that's associated with schizophrenia or bipolar disorder in a pediatric patient? And I think what we've seen in recent years, and there's empirical backing to this, is much greater recognition of catatonia in the pediatric population.Possibly greater actual occurrence of catatonia in the pediatric population. Unquestionably greater recognition.

There was a study that came out of Boston Children's just last year where they looked at consults to their CL service, between 2018 and 2022, and then between 2022 and 2025, and looked at what percentage of these ended up being diagnosed with catatonia. And in between the two time periods, the number of patients diagnosed with catatonia tripled in the pediatric population. Vanderbilt did a similar study and found a tenfold increase in catatonia.

Now, what to make of these numbers is not entirely clear. It shouldn't be surprising that when you develop diagnostic criteria for something, as we did in 2013, that eventually that filters into the community and then people start diagnosing it more. So, some part of it must be increased identification. But there's also more attention, I think, now to neurodevelopmental disorders. There's more attention to autoimmune diseases that occur in childhood, and there's more understanding that those often manifest with catatonia. So, recognition of diseases independent of catatonia that have it, right, as, a consequence is also increasing recognition.

But you absolutely see it throughout the lifespan, and I think that child and adolescent psychiatrists are increasingly getting exposed to catatonia. And this is actually, I think, the place, from my experience, where adult and child and adolescent psychiatrists have sort of the most interface because, historically, much of the training around catatonia is focused on adults, and we've been able to lend some of our knowledge and expertise about that to our pediatric colleagues.

Dr. Daniel Knoepflmacher: Can you just give me a, with confidentiality in mind, a example of an index case of a pediatric case that you were involved in that was a compelling example of this?

Dr. Leonardo Lopez: Yes, absolutely. So, we have taken care of several patients with NMDA receptor encephalitis, which is a disease of the young, has a median onset of around 21, and about three in eight patients are under 18 when they develop it. We've seen several patients here that presented initially with catatonia.

In fact, as a perhaps a slight digression, that condition presents, at the index presentation solely with psychiatric symptoms about two-thirds of the time. And about one-third of the time, the patients are actually admitted to a psychiatric facility when they present. So, I did have an example of this, maybe a year and a half back, was an 18-year-old that was seen in our CPEP and was noted to be psychotic and was thought to have first-episode schizophrenia and was admitted involuntarily to one of the hospitals in our service line.

And he became increasingly catatonic over the course of a very short period of time. He ultimately developed malignant catatonia, was transferred back to our ICU here, and, on CSF analysis was found to have, NMDA receptor encephalitis. So, this is probably outside the scope of this discussion. But in that case, there were a number of clues that this patient had catatonia due to a medical illness rather than a psychiatric illness. And we actually diagnosed him quite quickly. The average time to diagnosis is well over a month after presentation for these patients. So, diagnosing him within a week was quite quick. But there are many similar cases and, as I said, we've seen patients as young as five years old, presenting with catatonia as a consequence of autoimmune disease.

Dr. Daniel Knoepflmacher: You mentioned malignant catatonia there, and, it's important for everyone listening to understand that catatonia is a psychiatric emergency and, without treatment is dangerous. And so, can you talk about the risks, the complications that can occur when this is not diagnosed or treated effectively?

Dr. Leonardo Lopez: Yeah, absolutely. And malignant catatonia is the most extreme form. I'll save that for the end because, in general, it probably only constitutes about 1% of catatonia cases, although it's more common in medical catatonia. But before the patient gets to malignant catatonia, there are a lot of risks.

So, the primary medical risks are thromboembolic events, DVTs, from prolonged immobility, decubitus ulcers, also prolonged immobility, renal failure, as a consequence of muscle breakdown, and CK release into the bloodstream, and pneumonia, which typically happens as a consequence of aspiration because the patient isn't swallowing properly.

There's quite a bit of data on this. in fact, there's a great study from 2021 on the NMDA receptor population specifically that compared patients with that illness who were catatonic and not catatonic and looked at outcomes and found that the patients that were catatonic were 12 times as likely to have a DVT during their hospital course, were about five times as likely to have a decubitus ulcer, and were twice as likely to end up in the intensive care unit, usually as a result of respiratory failure, acute hypoxemic respiratory failure from aspiration pneumonia.

So, even before the patient gets to malignant catatonia, there are all sorts of risks, serious medical risks, potentially fatal medical risks of untreated catatonia. Then, of course, catatonia can progress to a malignant form, which you described before, which is a patient who still meets criteria, DSM criteria for catatonia, but is also quite rigid and typically has autonomic dysfunction, like you described before, either hyperthermia or abnormalities of the heart rate and blood pressure.

Often those are a very unique type of abnormality, which is to say that the heart rate and the blood pressure will shift very rapidly in very short periods of time from very high to very low. I recall the first malignant catatonia patient I cared for as an inpatient attending at another facility was admitted to me, obviously at 4:30 PM on a Friday. And showed up with agitated catatonia, running all around the place, disrobing, putting the pillowcase over her head, et cetera. And we settled her long enough to take her blood pressure, and it was 80/40. So, that was a freestanding psychiatric hospital, which meant we couldn't just transfer her to medicine. We had to call an ambulance to take her. Call the ambulance, ambulance comes right over. They measure her blood pressure, and it's 220/160. So, just very, very rapid shifts that you see often too, when you see this in the hospital, people will believe that it's user error. Like, they will see the heart rate go from 145 to 56, and they will say, "Oh, there's something wrong with the leads," right?

Like, the EKG's not on right or there's something wrong with the wires. And so, if you're the psychiatrist in that scenario, your medical knowledge is really important. You have to be able to say, "No, no, actually this is what we expect to happen in malignant catatonia. This is real and a really bad sign." That carries a mortality, even when diagnosed, and intervened upon of around 15%.

So, one in seven patients, very high mortality. So, very high-risk condition, absolutely a psychiatric emergency. You don't know who's that's catatonic will progress to malignant catatonia and who won't. About two-thirds of patients with malignant catatonia progress, meaning that they present as non-malignant and then develop malignant later. You don't know which are which, so you always have to treat it as an emergency because it can be lethal.

Dr. Daniel Knoepflmacher: And they go straight to the ICU.

Dr. Leonardo Lopez: It depends on the severity. Some of those patients go to the ICU. Some of those patients will go to step-down units. Occasionally, they'll go to floors. We sort of advocate for them not to be on the floors because these rapid shifts in blood pressure and heart rate are not things that can be picked up on the floors where they do vitals at intermittent ranges.

Often I think at our institution, these patients go to step-down, and then they will only go to the ICU in the circumstance where, for example, they aspirate and need to be intubated or their blood pressure drops so dangerously now that they need to be on vasopressors.

Dr. Daniel Knoepflmacher: There's so many more questions I want to ask, but I do want to turn to treatment. So, there's treatment for malignant catatonia, which is going to be different than—we already alluded to some of these in the introduction, but can you just talk about we've identified catatonia. It's been diagnosed. What is the protocol for treatment?

Dr. Leonardo Lopez: Two mainstays of treatment. You mentioned both of them in your introduction. One is lorazepam or Ativan, and the other is ECT. Ativan is a quite effective treatment for catatonia, and not infrequently when you give a patient with catatonia two milligrams of Ativan, you will see exactly what you described, where within a very short period of time, the patient is interacting with the environment again and perhaps even speaking.

Exactly how effective Ativan is, I think, a point of some contention, and I believe probably varies by underlying illness. It seems very clear that patients with affective disorders and catatonia do quite well with Ativan. Somewhere in the vicinity of three-quarters of those patients, Ativan will respond to Ativan.

The number is probably lower for schizophrenia patients and autism patients. There was at least one study in schizophrenia patients that showed Ativan not beating placebo for catatonia, although there were some design problems, but I do think it's probably the case that it's less effective. And also, in medical conditions, I think, we see it be less effective. Less effective doesn't mean ineffective. You'll see measures in medical catatonia, for example, of 45%, 50%, but does fail not infrequently.

And then, the secondary treatment that we will go to in a variety of circumstances, ones where Ativan has failed or has been insufficient or can't be tolerated or simply the patient is too ill for us to risk even trying, we will go to treat the patient with ECT. And ECT is and has been for quite some time, the gold standard treatment for catatonia. Depends on the literature you read. But suffice it to say, somewhere between 85% and 95% of catatonia patients will completely resolve with a course of ECT. And in fact, the literature we have suggests that that is true regardless of the underlying etiology of the condition.

In other words, patients with catatonia due to autoimmune diseases respond to ECT, and patients with catatonia due to bipolar disorder also respond to ECT. There are lots of other things people try that have sort of observational or case report level literature. Amantadine is one. Memantine or Namenda is another. I'm not super keen on those. Not because I don't believe there's a possibility that they work, but simply because we have a treatment that works so incredibly reliably, which is ECT. And the risk of using a treatment that doesn't work, as I mentioned before, is very high that patients really should progress to ECT, as quickly as possible.

So, just from a protocol point of view, I think we typically recommend that patients have something in the vicinity of 72 hours of a trial of six to eight milligrams per day of lorazepam. And if that fails, someone should be calling an ECT service. That doesn't mean that you can't go up on the Ativan dose. You can. Maybe it will help, probably not, but you can. It doesn't mean that you can't try amantadine or memantine too, but you should get the ball rolling on ECT if after 48, 72 hours you have not seen reasonable improvement with a reasonable trial of Ativan.

Dr. Daniel Knoepflmacher: I gave an example of a patient who responded well to treatment and then was subsequent to that point, wasn't dealing with catatonia, was dealing with primary treatment for bipolar disorder. That's not always the prognosis or the course for people who are being treated for catatonia. So, can you talk about maybe the more refractory side of this, and what the treatment range can look like for different folks with catatonia?

Dr. Leonardo Lopez: It's sort of similar to the hyperthermia example, right? So, you can usually find a way to cool the person down, but that might not solve the problem, right? Or it solves one problem, but not the major underlying problem.

So, we can usually, in fact almost always, eradicate catatonia in patients, at least for some period of time. That's one of the reasons why catatonia doctors like treating it. But the prognosis really is dependent on what is the underlying condition, right? And how does that respond to treatment.

One of the advantages of catatonia related to bipolar disorder or catatonia related to unipolar depression or psychotic depression is that those treatments independently respond to ECT, right? So, ECT will eliminate the catatonia while also treating the underlying condition. If ECT doesn't treat the underlying condition as effectively as it does those conditions, for example, in schizophrenia, or if it doesn't treat the underlying condition at all, like in autism spectrum disorder or an autoimmune disease, then the prognosis is much trickier.

I'll say that, for the patients we have with autism spectrum disorder who present with catatonia, I would say we are essentially uniformly effective in having their catatonia remit. However, they often remain on maintenance courses of ECT for a very, very long time. It can take a year and a half, two years to taper them all the way off ECT without their catatonia recurring, which is worth it because if their catatonia recurs, there's a lot of risk to that. But it can take a very long time simply because I think we believe that the underlying illness is so difficult to crack, right? And in autoimmune diseases, I think we are increasingly aware that, you know, we need some treatment for the underlying autoimmune disease for ECT to work.

The treatment for the underlying autoimmune disease often takes many, many months to be effective, whereas ECT can be effective for catatonia at least much faster. And we've seen this in our patients where they get immunotherapy, you would expect it to work over the course of many weeks to months. But then, we initiate ECT and, in fact, their catatonia resolves quite quickly. Whereas if they've received no treatment at all, if their treatment is ineffective, then we don't see the same response.

So, I think it depends mostly on what the underlying condition is. And again, I think, we can always handle it for a period of time. The real question is will it come back or not, and how hard do we have to work to prevent it from coming back? Which is related to what we're capable of doing with the underlying condition.

Dr. Daniel Knoepflmacher: So, someone with an NMDA receptor and encephalitis—really, again, back to what we were talking about with delirium, you're treating the underlying condition, in addition to continually treating the catatonia. But if that can be fully addressed, then it's a resolution. I mean, that's what you've seen in those cases?

Dr. Leonardo Lopez: Here's one way to think about it. This is the way that I tend to talk to our colleagues in other disciplines who are wondering why we would do ECT for autoimmune disease, because of course, ECT is a psychiatric treatment for psychiatric disorders. And my answer is sort of this, right? So, you know, if the patient presents in status epilepticus, you're not going to say, "Well, let's just give the person immunotherapy and then wait two to three months, and the seizures will resolve," right? You're going to give this person seizure medication because you can't afford for them to seize for two or three months.

And catatonia is similar in that regard, right? Of course, we're going to treat the underlying condition, but let's give something that we know is a symptomatic treatment for catatonia that will help it resolve faster and reduce the likelihood that they have this morbidity and mortality I described before.

Dr. Daniel Knoepflmacher: Yeah. No, and I think it's a nice analogy with status epilepticus, with a seizure disorder because another excitatory state caused by an underlying condition that in-intensely damaging if untreated. So, God, I'm going to have to cut out some of the other questions I wanted to ask you because both have to go to other meetings and things.

But we record this in the middle of our workday, so this is what happens. But I do want to just ask you maybe to sum up, what would be—let's think about two different audiences here. You know, for the general public and then for doctors and psychiatrists—I don't know if these are going to be the same or two different things. What would be key take-home points that you wish people knew about this condition, catatonia?

Dr. Leonardo Lopez: Okay. So for the general public, what I would like people to know is that it can present in many different ways, not necessarily the way that it's typically depicted in, right, film, literature, we described before, media, but many different ways. I think there are undoubtedly colleagues across the country who would agree there are undoubtedly many patients with autism who are experiencing catatonia.

Often this is diagnosed as a second regression or something of that nature, whose parents have no reason to believe they have catatonia because it doesn't look anything like what they've heard, right? So, I would like them to know that there are more ways that this can look, and specifically it can look like repetitive movements, and of course there's other explanations for that in autism. It can look like bizarre postures. It can look like all sorts of things. But the fact that someone is speaking and moving in and of itself does not mean that they don't have catatonia. They certainly could, under other circumstances. I think that's important.

I think the second thing I would say is that it's highly treatable. I mean, it's very difficult to think of really anything that we have in psychiatry that responds so robustly and consistently to treatment as does catatonia. So it's important as a consideration, and it's important perhaps even family members to broach it as a consideration, not because it's always there, because, most of the time it's not, but because if it's there, there's something we can do and we can, act on it quickly.

So maybe that's my general public piece. for physicians, I would say three things. the first is it's quite dangerous. I think that, that gets missed a lot of the time. that it's dangerous in that it causes the type of morbidity I described before. it's dangerous in that it can convert to a malignant state that, was actually initially called in the original papers in the early 80s lethal catatonia, right?

so it's very dangerous. second, I would say that it is a bridge between psychiatry and medicine, and people who see patients with catatonia, should not make the assumption that it is because they have schizophrenia or bipolar disorder. If you go onto YouTube and you, like, look for old-timey catatonia videos, they're always taken in asylums, right?

The idea is always that the person is deeply mentally ill. And physicians need to know that that's not n- in fact, 20% of the time that's not the case. A very high percentage of the time, right? if you see a patient with first-episode psychosis alone, overwhelmingly those patients have a psychiatric illness.

If you see the patient... Not always, but overwhelmingly. You see a patient with catatonia, one in five chance it's not a psychiatric illness. So, people need to know that. And then I'm going to change it to four things. I said three things. I'm going to do a fourth thing. The third thing is that, it is easy to miss, particularly in medical settings where people are not aware of it.

It's often confused with delirium, and it's often the cause of sort of untreatable agitation. So many patients that I get called to see that have been in ICUs for prolonged periods of time and on crazy regimens of propofol and fentanyl and Precedex that they can't sedate, they can't sedate because they have catatonia and they don't recognize the catatonia.

So that's the third piece. And the fourth one is related to that, which is that it's just super treatable. we can really, really, treat it to complete resolution almost always, sometimes with lorazepam, almost universally with ECT. And we've had a couple cases like this actually in our ICU at, Cornell where, you know, the patient has been on drips forever, and we've come down to the ICU and done ECT, and all of a sudden the patient's not agitated anymore.

those I think are, the four things. dangerous. It's not necessarily psychiatric. It may be the cause of the problem that you can't solve, and, we can solve it

Dr. Daniel Knoepflmacher (Host): Yeah. easy to miss, important not to miss, and really easy to treat, and very important, very important points. Leo, thank you so much for joining me again today to talk about this. It's an important and really fascinating topic, and I'm grateful not just because your knowledge and, expertise in talking about this, is great for a podcast episode, but it's also great for our residents who learn from you and for this amazing service that you've built here that's really made a tremendous impact in New York City and the region.

So thank you all you do, and thank you for coming on today

Dr. Leonardo Lopez: My pleasure. Thank you for having me. I, I was hoping we had five or six hours to

Dr. Daniel Knoepflmacher (Host): I know.

Dr. Leonardo Lopez: but,

Dr. Daniel Knoepflmacher (Host): we could've used it for sure.

like, I don't know. We, we have to do like a supplemental episode later. But, until then, I want to thank everyone else who listened to this episode of "On the Mind" today. this is the official podcast of the Weill Cornell Medicine Department of Psychiatry.

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