false
Catalog
Update on Catatonia
Presentation And Q&A
Presentation And Q&A
Back to course
[Please upgrade your browser to play this video content]
Video Transcription
Hello and welcome. I'm Dr. Rob Cotez, an Associate Professor in the Department of Psychiatry and Behavioral Sciences at Emory University School of Medicine. I'm also a member of the SMI Advisor Clinical Expert Team. I am pleased that you are joining us for today's SMI Advisor webinar, Update on Catatonia. SMI Advisor, also known as the Clinical Support System for Serious Mental Illness, is an APA and SAMHSA initiative devoted to helping clinicians implement evidence- based care for those living with serious mental illness. Working with experts from across the SMI clinician community, our interdisciplinary effort has been designed to help you get the answers you need to care for your patients. Now I'd like to introduce you to the faculty for today's webinar, Dr. Andrew Francis. Andrew Francis is a Professor of Psychiatry, Associate Director of Residency Education, and Director of Neuromodulation Services at the Penn State School of Medicine at Hershey Medical Center in Pennsylvania. He was the co-developer of the Bush-Francis Catatonia Rating Scale, published in 1996, which is generally recognized as the standard clinical and research tool to detect and quantify catatonic symptoms. This scale has been translated into several languages and used worldwide. He is a recognized authority on neuroleptic malignant syndrome, ECT, and delirium as well. Dr. Francis is widely published in these areas and has presented at regional, national, and international medical conferences, as well as serving as an invited lecturer at many major academic medical centers. Dr. Francis, thank you for leading today's webinar. Thank you very much, Dr. Coates, and also thank you to the SMI Advisor Program and its sponsors. I have no disclosures, and there will be some talk of non-FDA-approved treatments for catatonia. There are no approved FDA treatments for catatonia. So the objectives for today are listed here, and these are the goals for today's presentation. So catatonia was first described in the 1870s by Karl Kellbaum, who was a psychiatrist in Eastern Germany, and he published a monograph in 1874. It was translated into English in 1973, and he describes in this book beautiful case histories of unusual patients that he'd seen, and these are some words from the introduction. Patient remains motionless, without speaking, devoid of any will to move. That's the severe, retarded, or withdrawn form of catatonia. Impressions conveyed as of one of mental anguish or immobility. Tends to be persistent, although in some patients it can come and go, and Kellbaum, who first described it, also noted it was associated with medical, and what he's calling here muscular, we would call them neurological disorders. So Kellbaum had the idea that this was a specific disorder associated with medical illnesses, generally with a good outcome. Later, this is about the historical nosology, the diagnostic home, so to speak, that catatonia was assigned to. Later workers overly restricted catatonia to some type of schizophrenia, and in the German phenomenological tradition, represented by Kleist and Leonhardt and their followers, there are several types of catatonia identified. These aren't diagnostic systems recognized by the ICD or the DSM system. American workers, including Abrams and Taylor, emphasized that catatonia is actually quite associated with affective disorder, depression, bipolar. And Gellenberg published a series of papers associating catatonia with medical and neurological illnesses, and also drug toxicities. The DSM series, until recently, limited catatonia to being coded under schizophrenia. And in the current system, which I'll talk about a little bit more, the DSM-5 and the ICD-10, catatonia can be a specifier of other mood or organic diagnoses, as well as catatonia not otherwise specified as a provisional diagnosis. So is catatonia something that we still see? So in preparation for the DSM-5's efforts to consider diagnostic coding and descriptions of catatonia, we published this paper in 2010, which summarized 20 years of prospective studies of catatonia in adult inpatient psychiatric populations. These were all prospective studies using different methodologies to assess catatonia. Our paper was Bush et al., 1996. Most of the studies since have used our rating scale to assess the patients. And what this review showed is that catatonia is quite prevalent among acute adult psychiatric inpatient admissions, about 9% running across these studies, different ways of defining it, so to speak. And that the majority of these patients are going to be challenging to work with because they will have mutism, which means they don't speak or hardly speak at all. And they also will have negativism or withdrawal. Withdrawal means they don't interact with the environment. Negativism means they resist attempts to engage them with the environment. So they're largely going to be not speaking and also not engaging with the environment, which means it's difficult to arrive at a treatment plan and a diagnosis because they're largely not speaking or moving other than to recognize that they're catatonic. And so this was our effort to persuade the DSM that we needed at least a provisional diagnosis code for catatonia. So patients who are presenting with catatonia, just as someone who might present with new onset psychosis, there's a differential diagnosis of that. So there are a variety of metabolic disturbances that can present with a catatonic syndrome. Inflammatory conditions like systemic lupus erythematosus, metabolic disturbances like uremia, porphyria. We had a case of thyroid disease, thyrotoxicosis associated with a catatonic reaction. Neurological disorders, both generalized neurological disorders like encephalitis, but also focal and generalized seizures. We had a case of focal seizures who had unilateral catatonia. Toxic reactions, various drugs of abuse and also medications used in clinical care. Corticosteroids, so-called steroid stupor. Neuroleptics, antipsychotic drugs can occasionally produce a catatonic reaction. And neuroleptic malignant syndrome, our position from some studies is that neuroleptic malignant syndrome can be viewed as a drug-induced form of malignant catatonia. Malignant catatonia is that form of catatonia associated with fever and autonomic symptoms. And as well, catatonia is associated with a variety of psychiatric disorders, including affective disorder at all phases, depression, manic or mixed, psychotic illnesses, and also conversion disorder. So there's a broad differential diagnosis of someone who was presenting with catatonia. And certainly for the first time, they would deserve some medical or potentially neurological workup. Catatonia that's severe and persistent has medical complications. And these are mostly the complications of someone who is not moving, lying in bed or standing in one position. Things like aspiration pneumonia, pulmonary embolism from being dehydrated, not eating and not moving, rhabdomyolysis, muscle breakdown, respiratory failure, infections from aspiration pneumonia, or infected bed sores. So catatonia that is severe and persistent has medical complications, which are important things to be aware of and to consider, especially when catatonia is severe and persistent and are largely preventable. So over the years, we've been involved in several studies related to catatonia. Our early work was primarily designed at a systematic way to assess it. How prevalent is it? What are its characteristics? And the emphasis in that earlier period was on establishing catatonia as a clinical syndrome, a collection of signs and symptoms that occur together, persist together, and when it's reversible, go away together. And what are its clinical characteristics and its response to treatment? But over the years, we've looked at other studies looking at subtypes of catatonia, an excited form and a retarded form, and I'm going to show you videos, examples of these, acute and chronic, primary and secondary, and benign malignant. So there are considerations of subtypes of catatonia. Also, we looked at whether you can discriminate catatonia from other syndromes, motor syndromes, such as Parkinsonism or akathisia or dyskinesias. And the short answer is yes, you can. Some work addressing the question of is neuroleptic malignant syndrome, can it be usually viewed as a drug-induced form of malignant catatonia? And again, malignant catatonia means catatonia associated with autonomic symptoms like fever and elevated or labile blood pressure and heart rate. And then this last aspect is something that's intrigued us in recent years, and I'll talk a little bit about this towards the end, which is the interface of delirium and catatonia. So we published a rating scale about 25 years, almost 25 years ago now, and this was the first attempt really to have a systematic standardized method of assessing catatonia and also for systematic efforts at treatment response with a quantitative outcome and response to treatment. And this rating scale has been translated to several languages and it's used really worldwide and in many clinical centers as well as in research. So catatonia is a clinical syndrome, at least that's our position, and it consists of signs and symptoms. One of those is mutism, a classic catatonic sign that patients don't speak. And we wanted in our rating scale to be able to use the scale both for making a diagnosis and also for rating the severity. So we're going to make a diagnosis based on the number of signs and symptoms, as psychiatric diagnoses are traditionally made, and we're going to rate the severity by looking at the severity of each of the items on our rating scale. So in the case of mutism, how many words does a patient speak in five minutes? Do they speak no words at all? Do they speak less than 20 words or do they just speak in a fairly comprehensible whisper? So we arrive through a process of literature review of 23 items to define catatonia on our rating scale. Most of these signs and symptoms of catatonia come from Calbom in this 1874 book. Others were added by later workers. And 23 seemed like a reasonable number to have a workable rating scale that would be clinically useful but also comprehensive enough for research work. And of the 23 items, we included among the first 14, the most classic and commonly described catatonia signs. And they're also overlap highly with the DSM-5 list of catatonic signs. So in our research, we wanted to capture the milder cases. So the question is, how many signs and symptoms define a syndrome? And so we use a low bar in our initial research of two, only two items present out of the first 14. So we're going to define a case by the number of signs and symptoms, two out of the first 14. The DSM, which came later, has a similar list, 12, and they're shown here with the stars. And the DSM concept uses three out of 12. So if you assess the patient using the Bush-Francis rating scale or the DSM-5, they highly overlap, 90, 95% agreement on the patients that you're going to identify. And so we're going to define a case by at least two of the first 14 items present and on the DSM, three items out of 12. And we're going to rate the severity by taking all 23 of these items and rating them on a three-point scale. So caseness or diagnosis is at least two signs present and severity is going to be rating all 23 items on a three-point scale for each item. So the maximum score would be 69. This is very similar to the PHQ, for example, where a diagnosis is made by at least five things present and the nine and severity is by rating all nine items on the PHQ-9 on a three-point scale. So it's the same concept, using a scale to both make a diagnosis and rate severity. We also attempted to operationally define each one of these various catatonic signs. Some of them have German names from the German tradition of phenomenology. So for example, Gaggen-Holten. Gaggen-Holten is an abnormal motor tone that you assess by flexing and extending the elbow. And Gaggen-Holten is characterized by motor tone that increases during the arterial movement. Here's the list of the items on the DSM-5. It's a very similar list to ours. And the DSM-5 makes some attempt to define these items. I think our rating scale, which is freely available on the web, if you type catatonia rating scale into a search engine on the web, you will find the Bush-Francis catatonia rating scale and its definitions of all the catatonic signs. I think our definitions are a little bit better than the DSM-5. We also devised a standardized way to assess the patient. And that was in the attempt to improve the reliability of the exam. So some catatonic signs are observational. You observe the patient, you don't do anything except look at them. Examples of catatonic signs that you might see by observation are abnormal speech. So they don't talk at all. That's mutism. Or they talk in a repeating fashion, and they talk in a repeating fashion, and they talk in a repeating fashion, and they talk in a repeating fashion. That's verbiagration. Or they may have some unusual repetitious movements, things like mannerisms and stereotypies. And I'll show examples of that on the video coming up. Some catatonic signs or activity level, they stand or sit in one posture for many hours or an extended period of time without moving. That would be immobility. Or they're extremely hyperactive and move around constantly in a purposeless fashion. That would be excitement. Those are also catatonic motor signs. Some catatonic signs are elicited. So some are observational, some are elicited. So an example of an elicited one would be echopraxia or echolalia. Echopraxia is the patient mimics the movements of the examiner. Echolalia is the patient mimics the speech of the examiner. So the examiner might scratch his head, and the patient would repeat that movement without being told to do so, or repeat the speech echolalia. And that will be shown on the video. Some catatonic signs are, as I mentioned, observational, elicited, some are by exam. So there's three abnormalities of motor tone, rigidity, waxy flexibility, and Gaggen-Molten, which are defined on the rating scale. And those are assessed by flexing and extending the elbow. So with this operational definitions of these catatonic signs and the standardized way to assess them, there's a very high reliability of the rating scale. So what's shown on the left panel is use of the scale for diagnosis. Diagnosis, again, was going to be by the number of items present out of the first 14. Two would define a case or greater. And these are two independent raters rating the same patient, 44 ratings before, during, and after treatment. And there's a high correlation between the two raters' assessment of number of signs present. That would be for diagnosis. On the right-hand side of the panel is the two independent raters now doing a full rating scale score for severity. And again, there's a high agreement. So there's a high correlation. The kappas for agreement were 0.73 and greater. So it has good psychometric properties in terms of being able to reliably assess catatonia, which is what you want for a rating scale. So I'll show you now a couple examples of some patients with catatonia. So these are historical videos that are in the public domain. And I took them. They're posted on my website, www.catatonia.org, which is a catatonia information center sponsored by Penn State University, where I work. So this first patient is a patient from the 1930s. And he's showing a very classic example of a person with severe, withdrawn, or stuporous catatonia. And you'll notice what's being shown here and emphasized is rigidity of his posture. He's got a very rigid posture when the doctor attempts to move him around. He's got a vacant blank stare. He doesn't seem to look at the examiner. He's just sort of looking straight ahead. He's withdrawn. He doesn't seem to engage with the environment. He doesn't speak. And he has catalepsy. Catalepsy is the maintenance of a posture or a position into which he's placed. So his arm remains in an upright posture where it was previously placed. And you can see that the examiner moves the limbs and they stay in unusual postures, which may persist for long periods of time. And notice how the whole body seems to be rigid. There's no fluidity at all to the man's posture. He may remain in this unusual rigid posture for extended periods of time. He's not talking to the examiner. He also shows mutism, another catatonic sign. And he's blankly staring, not really engaging with the examiner who is moving him around. We'll see a close-up of his face here. And you'll notice that he's blankly staring. He's mute. He doesn't engage with the examiner. So it's staring, mutism, withdrawal, rigidity, and catalepsy. Multiple catatonic signs that are... So this man shows a very severe form of the stuporous or withdrawn form of catatonia. Fortunately, most patients are not so severe. And it's important to emphasize that he pays no attention, has no engagement whatsoever with the examiner, despite the examiner poking him and moving him around. So that's a catatonic symptom called withdrawal. So this would be a very gross form of catatonia that would be hard to miss. So there's a hyperactive form of catatonia as well, where the patients are overall physically hyperactive, sometimes extreme excitement, and they have repetitious movements or repetitious speech. And this man is an example of that. So he's an example of what I would call mannerisms, which are repeated movements that seem odd the first time you see them. Stereotypes are also repeated movements, but the nature of the abnormality is in the frequency, not the nature of the movement. So mannerisms seem odd the first time you see them. They commonly involve parts of the body used for communication, like the hands and the face and the upper body, and they're repeated, often in a sequence, as if to have a private meeting or a ritual for the patient. Stereotypes are repetitious movements where the abnormality is in the frequency, not the nature or context of the movement. So example would be rocking. And also shown is that he's overall hyperactive. His whole body moves, not just his hands. And he has grimacing as well. Grimacing is another catatonic sign. You might think of this as stereotype movements or posturing of the muscles of facial expression. Calbom called them schnauzkrampfen. In English, that would be snout cramps. So you'll see he's got sort of a sequence of movements that he does. He touches himself and his coat and his chest and his hand. He also moves an object back and forth between his hands, and he's overall in constant motion, not just his hands, but the rest of his body. So there's sort of a ritualized set of movements that he's doing, maybe in a certain sequence and a certain order. And you can see if you look closely at his face, he's grimacing, which is these stereotype repetitious movements of his lower face. So he's an example of someone who has a hyperactive form of catatonia, which would include, in his case, mannerisms and grimacing and overall hyperactivity, a mild case of excitement. Another hyperactive form of catatonia is characterized by echopraxia and echolalia. As mentioned, echopraxia is the patient repeats the movements of the examiner. Echolalia is the patient repeats the speech of the examiner. So here's an example of a woman sitting next to a doctor, and she's sitting in the same posture as he is, and when he moves his hands around or his body position in certain ways, she does the same without being bidden to do so. In a sense, she's mimicking his posture. So if you see here, the posture he's sitting in is very similar to the posture that she's adopted in terms of the knee, the elbow, and the hand on the face. So she mimics his movements and also his posture imperfectly, but quite a bit. And she does so in sort of a boisterous, overzealous way, so to speak. So I would say that she has echopraxia, quite prominent example of which. She might also have echolalia. We don't know. It's a silent movie repeating the speech. And she's, in a sense, overall hyperactive. She's much more fidgeting around and moving than the doctor is. So we applied our rating scale to an inpatient population at my former institution in New York to get a prospective cohort to learn about treatment and outcome. So we prospectively identified 28 adult psychiatric patients with catatonia. And the first thing was, again, we were trying to establish catatonia as a clinical syndrome. So when we prospectively rated all the consecutive adult admissions to the adult psychiatric unit, what we discovered was a frequency distribution of catatonic signs. So we screened 215 consecutive admissions over a six-month period within 72 hours of admission. The vast majority of those patients, 192, had none of the catatonic signs. Eight people had one catatonic sign on our rating scale, and this was commonly either excitement or withdrawal. Those are two catatonic signs, but in isolation, withdrawal can be seen in people who are depressed and excitement can be seen in people who are manic, but they didn't have other catatonic signs. Nobody had two. Remember, two was going to be our cutoff. And then we have a group of patients who have multiple catatonic signs, and this was out of the first 14, and they had an average of six. So this was helpful in our efforts to validate the idea that catatonia was a clinical syndrome. It can be identified as patients distinct from the overall group of psychiatric adult patients in patients who have multiple catatonic signs. So most of the patients won't have these things, and then there's a cluster of patients that do. So this is good evidence along the way of establishing that catatonia is a clinical syndrome. It's a collection of signs and symptoms that occur in patients distinct from other patients who don't have it. What about association with psychiatric illness? So Kalbaum, when you look at his cases where there's enough description to arrive at a possible diagnosis, the majority had affective disorders, things like depression and mania. American workers, including Abrams and Rosebush, associated catatonia with affective disorder primarily, by the way, bipolar disorder, manic phase. And our study of the 28 patients, 15 turned out to have affective disorder. These were diagnoses arrived at once they became, once their catatonia was relieved and they were able to be interviewed and were able to speak and engage in behavior to allow a diagnosis to be made. So when prospective studies of catatonia are assessed, patients in a high rate turn out to have affective disorder. Going the other way, screening people who are identified as having mania, depression, and assessing for catatonia, there's also a significant proportion of them who have catatonia. So looking at this from either direction, there's an association of catatonia with mood disorders. What about other populations? So there's increasing recognition of adolescents, especially those with neurodevelopmental disorders of having catatonic features. And here are a couple of chart studies and prospective studies looking at adolescents with autism and catatonia can be present in a significant percent. In geriatric patients, Starkstein, a study of people referred for depression, geriatric population referred for depression, 20% at catatonia, and in our study, geriatric population with schizophrenia, 21% had catatonia. So what about treatments for catatonia? There's no FDA-approved treatments. Any treatments are off-label. Many of them have very good evidence base for them. There doesn't seem to be a placebo response, although only one small study using sodium amobarbital, so-called sodium amobarbital interview, in the early 1980s, and that was a short-term trial of 10 minutes, included a saline infusion. And the saline had no response, and the amobarbital had a good response, very similar to lorazepam as nowadays that we use. Convulsive therapy, it got its start because the patients that they tried it on had catatonia, and catatonia is highly responsive to convulsive therapies, things like ECT. Neuroleptics. There's some evidence that neuroleptics make catatonia worse, perhaps precipitate a malignant form of catatonia called neuroleptic malignant syndrome, especially the older, high-potency first-generation antipsychotics. There's a variety of case literature of miscellaneous agents that might improve catatonia. Benzodiazepines are the most common first-line agents used in contemporary practice. Examples of open trials, including the one I'm going to tell you about, no double-blind controlled trials, and everyday experience as well. So this is one of those things in medicine, in psychiatry in particular, that is an everyday experience that lorazepam is highly effective for catatonia, as is ECT, but neither has been subjected to double-blind controlled trials. Benzodiazepines, including lorazepam, are GABA-A agonists, and an alternative GABA-A agonist, zolpidem, marketed in the United States as a sleeping pill. There's open trials of this in medical and psychiatric populations, and it seems to be almost as effective as lorazepam, but it tends to have a short-term response. There's some evidence that NMDA antagonists, like imantadine and imantine, might be helpful, and there's an uncertain role of atypical antipsychotics. Some case literature is suggesting they make it better, some that they make it worse. So back to our protocol and our cohort of patients, there were a couple of case reports at the time that intravenous lorazepam might work for a neuroleptic-induced catatonia, but it hadn't really been systematically studied in a quantitative fashion with a validated rating scale. So we used lorazepam, ideally intravenously if we were able to, and then lorazepam by any route, oral, intramuscular, IV, for up to five days in a dose range of 4 to 8 milligrams. In retrospect, this is underdosing. We've learned since that some patients require higher doses of lorazepam, not on the first day, of course, but titrated up, and we assessed them by daily ratings. Success was, did they no longer meet criteria? Again, our criteria was two signs present, and failure would be they got worse or they became agitated or worse clinical status. So with respect to the intravenous lorazepam, we had 11 patients that we were able to do intravenous lorazepam, and what's shown on the y-axis here is the full scale of rating all 23 items on a three-point scale, the Bush-Francis catatonia rating scale. So the typical hospital patient is going to score somewhere between 15 and 25, typically. Maximum could be 63. 23 times 3 is 69. 69 would be the max. Typical patient is 15 to 25 that you might see in a psychiatric hospital or on the medical floor. And what's on the x-axis is the baseline severity score of catatonia, and then after one dose of lorazepam, one milligram at five minutes, and then after a second dose five minutes later, another one milligram. So this is a 10-minute clinical trial of intravenous lorazepam for catatonic patients on a psychiatric unit and with two milligrams total of lorazepam. And what you see is that about 50% drop in the catatonia severity, a little bit more substantially, over 10 minutes. And that's variable. It's statistically significant at both times. And this became the basis of what's now known as the lorazepam challenge test, which is used both to confirm the diagnosis and to start a treatment. And it's commonly used in medical and psychiatric facilities around the world. The treatment response was variable. Some patients, the catatonia resolved. Some patients had no effect. But on average, you will see a significant effect from intravenous lorazepam. About two-thirds to three-quarters of the patients are going to have a good response to the lorazepam within the first few days of treatment. So when we carried that treatment trial out for five days, what's shown here is the five-day trial on the x-axis from baseline, and what's shown on the y-axis is the catatonia severity scale rating all 23 items on the three-point scale each. So the typical patient is 15 to 20. So what's shown here is some patients, and ours, we had 21 patients who were able to conduct a five-day trial of lorazepam. Sixteen out of the five responded well, and the catatonia completely resolved by five days of lorazepam in the dose range of four to eight milligrams per day. However, there were some who did not respond. So this is about 16 out of 21. That's about 75% had a good response, but about 20, 25% don't, and that's been confirmed multiple times since that about two-thirds to three-quarters of patients will respond who have catatonia will respond to lorazepam, usually within a few days. We also learned that if the patient is going to respond to lorazepam, you tend to see at least a partial effect within the first day or two, but there are some who are just resistant to lorazepam. What were the characteristics of those who responded and those who did not respond? Basic demographics were not a factor. The catatonia severity, surprisingly, was not a factor either. So someone who has a very severe catatonia form based on the severity of the scale or a milder form of catatonia, but still meets criteria, they have an equally good chance of responding to the lorazepam. Bipolar disorder didn't make a difference. Not surprisingly, duration of catatonia made a difference. The longer you have something, the more difficult it is to treat. As I mentioned, the percent drop in the score of severity on the first day was a particular ultimate outcome. So even a partial response on the first day is a good sign that the patient will eventually respond. And the dose didn't seem to predict response, although in retrospect, this was underdosing. All of these findings have been confirmed in later studies. Patients who did not respond to lorazepam, we were able to do ECT on four of them. And that was bilateral ECT with age-based dosing. We stopped all medicines. In retrospect, we learned later that low dose lorazepam is synergistic with ECT. And what we find there was these are four patients now who failed lorazepam, and now they're able to do ECT. And most of the patients respond to just a few ECT treatments. There was one patient, a bit unusual, he took several treatments to have a full response. So ECT has a very good treatment response outcome for catatonia. 90 plus percent of patients are going to respond to ECT, even if they fail other agents like lorazepam or zolpidem. Or if they have a medically induced catatonia and the medical, quote, cause, unquote, has been corrected, but they remain catatonic, they can still have a good response to ECT, provided they can tolerate the ECT. So more recently, I've been working in collaboration with other workers at other universities on the interface between catatonia and delirium. So I would occasionally cover the consultation service at my former institution in New York, and we would see people who were in the ICU or in the medical floors who were delirious, but also seemed to have some catatonic features. So we published an article about 10 years ago, kind of provocative, so to speak. Is there such a thing as delirium with catatonic features? So in the literature on delirium, there are subtypes of delirium called a hyperactive form and a hypoactive form. And we reviewed some of that. We also reviewed some literature on the biological differences between this hyperactive and hypoactive form of delirium, in terms of some biological measures and also some treatment outcome measures. So looking more closely at this definition of hypoactive or withdrawn form of delirium by different researchers and how they defined it. So for example, this first one, the confusion assessment method, that's Dr. Wes Ellie from Vanderbilt, the CAM, the confusion assessment method. It's an assessment method for catatonia. This description of hypoactive delirium, decreased motor activity, sluggish, staring, staying in one position, moving very slowly. So looking at that through the lens of a person that studies catatonia, well, this sounds like immobility, staring, and posturing. Another one is the delirium memorial delirium assessment scale. That's Dr. Breitbart from Sloan Kettering. Increased or slowed movements, rarely moves or speaks, is catatonic. And that would potentially map onto catatonic signs of mutism and withdrawal. So it looked like this withdrawn form of delirium, maybe some of these patients in fact are actually catatonic, and this may have a treatment or a prognosis implication. And we were able to identify three patients in our hands at our hospital, and a literature review showed an additional 13. So we had 16 patients who met rigid research criteria for catatonia by the Bush-Francis and the DSM, four at the time, and also met research criteria for delirium concurrently. So these were patients who met criteria for both delirium and catatonia all at the same time. And what we discovered was that they had multiple catatonic signs. So this was a hint that there is such a thing as delirium with catatonia. Catatonic features are an interface between delirium and catatonia. I was unable to persuade my consultation service to do a prospective study, but another researcher in India, Sandeep Grover and his colleagues, were inspired by this article and did do such a study. So they're in an academic medical center, and they looked at 205 consecutive consultation liaison referrals. These are med-surg patients being seen by a psychiatry consultation service. And they assessed delirium by the TRAPAS delirium rating scale, and they assessed catatonia by the Bush-Francis, and they made a diagnosis by DSM-5, which, misprint there, requires three out of 12, or Bush-Francis, two out of 14. So these were prospectively identified, systematically rated, and confirmed to have delirium and catatonia. And what they found is that, again, the DSM-5 requires three signs, it's a little more stringent than the Bush-Francis, two out of 14, that anywhere from 13 to 32% of these patients who are prospectively identified and rated as having delirium had catatonia and delirium both, and that the severity of the delirium rating scale and the severity of the catatonia rating scale correlated. That is to say, the more severe the delirium, the more catatonic signs and symptoms they had. And they typically had this hypoactive form of delirium. So this was prospective confirmation of the idea that there's an interface between delirium and catatonia. And shortly, a few years later, Joellen Wilson at Vanderbilt, who was a resident consultation fellow and now a junior faculty, did a prospective trial in the delirium research projects that Dr. Wes Elly, who's also at Vanderbilt, has been conducting for years. So this was a prospective outcome trial of delirium in hospital patients who were primarily older patients who had sepsis or respiratory failure and entered the ICU. So this was a big study of delirium outcome. And Joellen Wilson was able to add catatonia ratings onto this study. So these were patients prospectively assessed for onset of delirium in an ICU. They weren't delirious to start. And what were the factors and predictors of onset of delirium? And she was able to add blinded catatonia ratings to these prospectively identified patients entering an ICU at risk for delirium. And what she found, and I'm a co-author with her on this project, is that in the sample of 136 people prospectively identified entering ICU for a development of delirium, not surprisingly, 42% developed delirium. You'd expect that in a population of medically sick patients entering an ICU. But 30% had both delirium and catatonia, or a small percent had catatonia alone and a significant percent developed neither. So again, this is confirmation that some patients who have delirium also have catatonia. So the implications of this for prognosis, is delirium with catatonic features worse in terms of prognosis or bad outcome from delirium than delirium without catatonic features? Does it have an implication for treatment? That is to say, we normally avoid benzodiazepines like lorazepam in delirium, but might we give patients with delirium who also are catatonic benzodiazepines? And should we avoid antipsychotic drugs in patients with delirium who also have catatonia? Because we know antipsychotic drugs can make catatonia worse. We can talk more about this in the Q&A portion. So to summarize, I've presented evidence and have been working for years to establish catatonia as a distinct neuropsychiatric syndrome that can be reliably detected across a variety of comorbid diagnoses, both medical and psychiatric diagnoses, including mood disorders, developmental disorders and delirium. It's heterogeneous, there's subtypes, so to speak, a hyperactive, a hypoactive form. It's correlated with affective disorder and mania, as well as certain medical conditions and toxicities. The diagnosis should be based on the number of operationalized signs. In the Bush-Francis, it's two out of 14. Although what we've learned in the populations, studies with populations in medical patients that a stricter criterion of perhaps four signs in the medically sick population is better than two signs in terms of sensitivity and specificity. The DSM-5 methodology is not bad for making a diagnosis. Lorazepam is an effective initial treatment. Zolpidem is a secondary option and there's a variety of third and fourth line agents. An uncertain answer to a question is the role of atypical antipsychotics. There's some case literature and case theories that they're helpful, there's some that it's harmful. There seems to be a risk of neuroleptic malignant syndrome when using antipsychotics, perhaps even with atypicals. There's a close relationship with neuroleptic malignant syndrome. And as I mentioned, we've published quite a bit on the idea that MMS is a toxic or drug-induced form of catatonia, malignant catatonia. And laterally, what we've been intrigued with is this idea of delirium with catatonic features. What might be the implications for this in terms of the prognosis and treatment of delirium with and without catatonia? So I'll stop there and I hope we can have some time for questions. Thank you very much for having me. Okay, Dr. Francis, thank you so much for such a wonderful talk. And now we want to give the audience some time to ask some questions to Dr. Francis. We've already gotten some questions from the audience so far, and maybe we can go ahead and get going with those. So Dr. Francis, the first question I have for you is, are there first-person accounts of individuals that have experienced catatonia and what are those like? So the question is about what is the mental experience of someone who's catatonic? So the gross form of catatonia that I showed on the video, that person is sort of frozen and rigid and mute and not engaged with the environment and gives the impression of being, give you an impression of being distressed. And Calvon talked about this. There's been a couple of workers. There's one systematic study. And so, but people, most people who are catatonic aren't able or are withdrawn and don't engage with the environment. But once they do, they can retrospectively often describe what their experiences were while being catatonic. And that's quite variable. Some will say, I felt extreme anxiety or I was tense. Sometimes they give a psychotic explanation. The voice has told me not to move or talk. Sometimes they say, I couldn't move or talk. I tried to move and talk, but I wasn't able to for some reason. And sometimes they give a very superficial or facile account. Boy, I was resting or I just felt out of it. So they sometimes don't give a very satisfying answer, but sometimes they do give a experience that's unpleasant. They are also awake. This is not a metabolic stupor that you might find in the ICU. It's a psychological stupor, so to speak. And they will recall, you were the doctor with the red tie. They will recall events typically that happened during this episode. Thank you so much. And as a follow-up to that, I'm kind of wondering what as clinicians can we do if we're working with someone who's experiencing catatonia to help people feel more comfortable or if they're not feeling safe, helping them to feel more safe? Well, the most important thing, so my answer to that is two things. The most important thing is to recognize that the person is catatonic and then start working on some sort of a treatment or workup to help them. And while that is happening, to be very supportive and reassuring. They're not in a coma. They are awake, alert, and sometimes tense and anxious. And to be very reassuring and supportive and to tell them you're having difficulty now. What you're experiencing is something that's very difficult, but we're able to treat it. You're gonna be able to feel better. Soon. All right, thank you so much. I wanted to move to the next question. This was from the audience and the person mentioned that they learned earlier in their career that a person with catatonia would stare and not close their eyes. They recently had a spirited debate with the consultation liaison service about this. And what are your thoughts about that? Well, so the question is they often have staring. It's one of the common catatonic signs that's on our rating scale. And it's often a sort of a blank stare. They tend not to stare at people. Sort of a blank, vacant stare. Not necessarily seeming to focus on a particular target in the environment. And generally speaking, not the people around them. And they do have decreased blinking, I would say. But to the point of corneal drying, I think that's unusual. Okay, thank you. The next question, Dr. Francis, is can you comment on the use of atypical antipsychotics in catatonia with people who are experiencing psychosis? Yes, so sometimes, so if somebody has a problem in the case of catatonia, they're usually withdrawn and not talking. So you don't know for sure if they are psychotic until you're able to relieve the catatonia and they begin to talk and behave. And then you have a better behavior pattern and mental status exam to allow you to make a diagnosis or at least a conclusion that they're psychotic or manic or depressed or potentially delirious. And then a question arises how you would treat those associated syndromes. So in the case of depression or mania, you can use mood stabilizers and antidepressant drugs. They don't seem to make catatonia better or worse. The problem arises when somebody is psychotic who has been recently catatonic or has some residual catatonic symptoms that don't seem to respond well to the racepam and ECT is not available or not feasible. And in that scenario, we do occasionally use antipsychotic drugs, but with great caution. And generally speaking, keeping the racepam, if that's what you're using, going and closely monitoring for extrapyramidal side effects and vital signs. So there's no systematic studies. There's case literature that sometimes atypical antipsychotics can make catatonia better and sometimes it can make it worse or precipitate a malignant form. So there isn't good systematic data on that, but in clinical care, it often comes up as a problem that someone who was catatonic is now no longer catatonic or minimally catatonic and is showing psychotic symptoms, what do we do? And the best treatment is really ECT if that's available, but if not, cautious use of various low dose atypical antipsychotics has been recommended, but there's no systematic data to support that. Thank you. All right, thank you. And of the atypical antipsychotics, I know that there's a real lack of data in this area, but are there certain antipsychotic medications you may think may be safer than others and does it have anything to do with the amount of dopamine D2 blockade? Well, I have used a low dose risperidone. I have used low dose olanzapine. There's one small study, a very small study, it's 14 subjects, half of whom got ECT and half of whom got risperidone. And total N of 14, it's not a big study, but it was randomized. And those were people whose catatonia failed lorazepam. And now the question is, can we give them either ECT or risperidone? And in that small study, they got a lot better with ECT, but the ones who got risperidone improved by 50%. So there's one small study that low dose risperidone didn't make it worse, but there's also other studies that risperidone precipitated worsening of catatonia. So the most practical thing is try to delay the onset of needing antipsychotics. And if one tries them to use extremely small doses and closely monitor vital signs and extrapyramidal side effects. All right, thank you. You know, another question I had was, I think that sometimes catatonia can be a difficult concept to explain to various clinicians. And I sometimes wonder, do you have any tips about how to explain catatonia to a person who experiences it? You know, sort of like, are there any resources that you can give them or are there any, you know, strategies that you use to sort of talk about catatonia and try and help people make sense of that experience, which can sometimes be quite scary? So for the patient or the family? Yes. So on our website, www.catatonia.org, there's information about catatonia, which could be useful for families. For the person who is acutely catatonic, while they're catatonic, they're not usually able to speak or engage with the environment or with examiners, but they can be offered reassurance that they're safe and that we understand that they're having difficulty and it may be frightening, but that we're able to help them. We do occasionally see people who have recurrent catatonic episodes. And there's usually, not always, but usually a symptom that precedes it, which they may monitor themselves for. So it's highly associated with bipolar disorder. So if they feel whatever their typical symptom is, so for some people it might be they're not sleeping or they feel racing, that might be a warning signal that it's coming and they might seek attention earlier. Yeah, I wanted to go back to that a little bit more. Can you speak to the natural history of catatonia a little bit? And if someone responded to a lorazepam challenge, how long do the benzodiazepines need to be continued? Well, it depends. So the question would be, it depends what else is, what other diagnoses they have. So sometimes catatonia occurs sort of on its own in association with nothing that you can discover, but most commonly it's gonna be associated with another psychiatric illness or a neurological illness or some sort of a medical illness or toxicity. So if it's associated with a medical illness, a neurological illness or a toxicity, so for example, corticosteroids that can induce a catatonic stupor, addressing those things or removing those things if it's toxicity, the lorazepam might not be needed for very long, days or weeks perhaps. If they happen to have a psychotic illness or a mood disorder, the catatonia is most likely during the active phase of those illnesses. And if they get out of a depressive or a manic episode, their catatonia is likely also be relieved. All right, thank you so much. I wanted to go back to some of the remarks that you had made on the overlap between delirium and catatonia and some implications for treatment there. Can you talk a little bit more about how clinicians should think about that and should, I know you mentioned a little bit about the considerations with benzodiazepines and just sort of what other options, what we think about. Right, so generally speaking, we avoid benzodiazepines and delirium because it tends to make confusion worse. With the exception of those forms of delirium that are clearly associated with things like benzodiazepine withdrawal or alcohol withdrawal, where the benzodiazepines and related agents tend to improve the delirium. And when we use medications for delirium, traditionally, they tend to be antipsychotic drugs, in particular haloperidol and related compounds that often improve the psychotic or agitation symptoms of delirium. Some question whether they improve the cognition, but tend to make catatonia worse. So there's a mismatch, so to speak. So now you have somebody who has delirium and catatonia both and prospective studies have now confirmed that this can exist. We don't for sure know the treatment implications of this. So if you have delirium with or without catatonia, does it presage a benefit of low dose lorazepam and a worsening with antipsychotic drugs? We don't know that. Hasn't been any data prospectively on that. There's a retrospective study from the University of Chicago that hinted at possible benefit of lorazepam when patients were both delirious and catatonic, but it's not really systematic prospective data. So we're looking for that. We're hoping people can try cautious doses of this and even in a case series format. So someone who's doing a consultation, excuse me, doing consultation work and sees patients with delirium and catatonic features, perhaps try a cautious trial of low dose benzodiazepines. An alternative would be some of the second line agents, one of which is memantine. And there's some case literature about memantine improving catatonia and also improving cognition. And we have a case report in press in psychosomatics of such a case where a person had cognitive impairment and delirium, kind of cognitive impairment and catatonia at the same time, and the memantine improved both. And there's a bit of a case literature on this. So alternative second line agents for catatonia that may also be cognitive enhancers, such as possibly imantadine or possibly memantine might be things that could be considered in that scenario of delirium with catatonic features. But we lack systematic information. And one final question. Yes. In your opinion, does catatonia always require hospitalization? No, fortunately, many cases of catatonia are mild and also intermittent. So there are examples of people who might be sitting or standing in a posture for some hours, but when lunch is, even in a hospital setting, when lunch is called, they walk down to have lunch, come back and resume their posturing. So some people with catatonia, if it's mild, can be maintained at home. The severe form of catatonia, where they're not moving at all and very rigid, there's medical complications of that. Bed sores, pressure sores, dehydration, and blood clots. But if a person is mildly catatonic and moving around, perhaps even talking at periods of time, theoretically possible they could be managed at home or on an ambulatory basis, let's put it that way. Thank you. I think that's such a good point that you made there at the end, especially if someone is not moving. It's important, I think, for inpatient psychiatrists or the other members of the treatment team to consider anticoagulation medications. Yes. People are really not able to move. Yes. Okay. So thank you so much again, Dr. Francis. That was the end of the Q&A section.
Video Summary
In the video, Dr. Andrew Francis discusses catatonia and provides an update on its diagnosis and treatment. Catatonia is described as a collection of signs and symptoms that can occur in various psychiatric and medical conditions. It is associated with depressive and bipolar disorders, as well as certain neurological disorders and drug toxicities. The diagnosis of catatonia is made based on the presence of specific signs and symptoms, with the severity of catatonia assessed using a rating scale. The most common treatment for catatonia is lorazepam, a benzodiazepine medication. Other treatments include electroconvulsive therapy (ECT) and certain antipsychotic medications, although caution is advised with their use. The video also explores the overlap between catatonia and delirium, suggesting that some individuals may experience catatonic features during delirium. The prognosis and treatment implications of delirium with catatonic features are still being explored. It is important to provide support and reassurance to individuals experiencing catatonia, as well as to monitor and manage any medical complications that may arise. Overall, catatonia is a distinct syndrome that can be reliably diagnosed and effectively treated using various approaches.
Keywords
catatonia
diagnosis
treatment
symptoms
depressive disorders
bipolar disorders
neurological disorders
lorazepam
electroconvulsive therapy
delirium
Funding for SMI Adviser was made possible by Grant No. SM080818 from SAMHSA of the U.S. Department of Health and Human Services (HHS). The contents are those of the author(s) and do not necessarily represent the official views of, nor an endorsement by, SAMHSA/HHS or the U.S. Government.
×
Please select your language
1
English