Psychiatry & Psychotherapy Podcast - Catatonia: Diagnosis and Treatment

Episode Date: February 15, 2020

Catatonia is a severe motor syndrome. It is a secondary response to an underlying illness that requires quick diagnosis and treatment. There are many different things that lead to catatonia, so finding out the underlying cause is very important. In this episode, Dr. Cummings and I discuss the history, diagnosis, and treatment of catatonia.  By listening to this episode, you can earn 1 Psychiatry CME Credits. Link to blog. Link to YouTube video.

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So welcome back to the podcast. I am joined with Dr. Michael Cummings. this is actually a second time we recorded. We had some technical issues the first time through. We are going to be talking about catatonia. And I think it would be really important, Dr. Cummings, to start with what are we actually looking at? Like, when we talk about catatonia,

like if someone did not know what catatonia was at all, like let's go through and describe it. Let's describe aspects of the history of it. Because this is something that in some studies, it says that 10% of acutely ill psychiatric patients, so patients who are in a psychiatric hospital, have been diagnosed with catatonia. Now, I don't know if that's as high in all institutions,

but yeah, so let's start with just the definition of what we're looking for. Okay, catatonia was first described in 1874 in Germany. Essentially, this is a motor syndrome that can be characterized by one of two states, either incredibly increased frenetic motor activity that is extreme and purposeless if allowed to continue unchecked

that will eventually result in collapse. And the other type, which is more common, is catatonic stupor, which is characterized by a slowing in speech and behavior, eventually, at its most extreme end, resulting in essentially a frozen motoric state in which the person is mute, unable to initiate movement, although they are, by their own report after recovery, aware of their environment while in that state.

Yeah, so the two classic principal signs are mutism and stupor. mutism is decreased speech, silent, unresponsive speech, and it's not always accompanied by stupor or immobility. And stupor, we define as persistently unresponsive, unaware of the surroundings, can be difficult to distinguish from mutism because, you know, someone who's in a stupor may not be as responsive. And they sometimes can move from there into. see something more energized for a few hours, something looking like manic excitement. But often what I've seen is that they're in this mutism and stupor, and then they may have some echolalia or echofenomena.

Do you want to talk about that? Yes. Anything I mentioned there? Yes, indeed. You know, the 10% figure that we started with reflects our best estimate of the overall prevalence of catatonia. In the extreme forms, that is, with fully developed catatonic excitement or catatonic stupor, it's fairly difficult to miss because of the profound nature of the syndrome.

People often, however, miss catatonia or catatonic symptoms in their more subtle forms. For example, with speech, it often starts with increased speech latency. The person responds, but there is an increase. length of time for their response to begin. That gradually evolves into a partial mutism where they respond sometimes, but not all the time, or echolalia in which they may simply repeat the last portion of what was said to them and then stop all the way to complete mutism in which there is no speech at all. and in many ways the motor activity follows the same course they often initially appear somewhat slowed

and that may evolve into holding unusual postures for extended periods of time to eventually being so frozen that they can be positioned by somebody else and they will stay in that position sometimes referred to as waxy flexibilities they kind of look like a wax figure that you can shape, but then they kind of do gradually respond to gravity. For example, if you put their arm up, it will stay up, but gradually, very gradually drift downward. One thing that we mentioned was echolalia,

which is that the patient repeats your or the examiner's utterances, and there's also echopraxia in which the patient spontaneously copies the examiner's movements, or is unable to refrain from copying the examiner's test movements despite instructions to the contrary. So you're saying that that might happen before mutism, or where does that happen in the trajectory of usually the progression? Those are earlier, milder signs, and they may start very subtly. Initially, for example, with echolalia,

the person may repeat the last words of the question or the statement, and then proceed to give an answer. But eventually that, as it becomes more severe, devolves into simply repeating the last few words. The same thing with echopraxia, where the person may tend to mimic occasionally the movements of the examiner, even when being told not to,

all the way to then that becoming a more complete mirroring of movements that then eventually gives away to loss of movement altogether. At what point in the disease do they stop eating, drinking, you know, they lose weight, may develop muscle wasting, contractures, bed sores? Usually that's toward the more severe end, often seen in conditions like major depressive disorder, melancholic depression, or in severe schizophrenia or severe schizophrenia or, severe bipolar depression.

When people reach that stage, it has truly become a medical emergency without treatment. These people will become unstable and essentially die of the catatonia. I did want to point out that catatonia is not an independent disease. Instead, it is a secondary phenomena that is always associated with an underlying illness. and that can be either a psychiatric illness, a neurologic disorder, or can in some cases, also be the result of things like benzodiazepine or alcohol withdrawal or other global metabolic disturbances. So the list of things that can be associated with catatonia is truly immense. So would you consider this something that should be treated in a psychiatric hospital or in a regular?

hospital or like at what point in the workup are we are we thinking okay this is just bipolar this is just depression this is just schizophrenia like and it's progressed into the catatonia in many cases you're guided by the prior history if this is a person who has a known diagnosis of a psychiatric disorder and they're now presenting with catatonic symptoms the psychiatric illness is the most probable underlying cause. I think even though in a psychiatric setting, certainly doing a neurologic exam and general labs, to look for things like evidence of infection or metabolic disturbance is certainly not unreasonable.

In most cases where it is the result of an associated neurologic or medical condition, often the onset is more abrupt. And the person does not have a past history of catatonic episodes unless they also have a history of recurrence of the same medical condition or neurologic condition. Very often in the general medical hospital, catatonia shows up in the context of an evolving delirium, secondary to metabolic or neurologic disturbance. Okay. So in the history of someone with Catatonia, like what I've seen, maybe let's start with depression,

is that, you know, the depression worsened over the last like three or four months or six months. And then all of a sudden they stopped talking as much. They had that delay in speech. So, you know, instead of responding right away, they responded in, you know, four seconds after. So they had kind of a delay. And then, you know, they stopped eating as much. So there's often like some weight loss. You know, and that all led to them being very concerned

and bringing them into the hospital. Yes. Yeah. Often by the time they present to the emergency room, usually with family, or to a psychiatric hospital for admission, the catatonia has at that point been evolving for some time. Again, in its early stages, the signs and symptoms can be relatively subtle.

In the severe stages, though, the person is literally shutting down. They look for all the world, like somebody whose batteries are running down and they're slowing down to a gradual halt. Yeah, I once saw a pretty severe catatonic patient with incredible stupor where it took them about 10 minutes to walk down the hall. like that's how slow they were and talking there would be probably about a five second delay and then very slow speech like dr pewter yeah that's exactly what they become like in terms of both speech and if you have them write their ability to write also slows down in conjunction with the speech those two things go together. So if you have them write a sentence or write their name, it will be an excruciatingly slow process. Yeah. And sometimes these people die from DVTs and pulmonary

embolisms because they're just not moving much at all. Yes. Often in forensic settings, these people will be reported by the correctional officers, oh, he stands for a long period in his cell just staring at the ceiling, which is an unusual behavior. And eventually that devolves into, as you've said, lack of eating, lack of fluid intake. And then, of course, eventually with that, the person becomes medically unstable. I had one patient, probably bipolar too, who stopped drinking and stopped eating. And he was in his primary care office, and he fell over because he was hypotensive. And they were having the hardest time working up his hypotension.

And then they came in and saw me at a, you know, increased interval because we were concerned about him. And he had these long delays in his speech and he was not talking much at home at all. And he was hypotensive from just not drinking because he just lost the urge or the normal drive to drink. Yes, and indeed, that's one of the reasons it's important to spot catatonia before it evolves to the severe end of its trajectory. There is a provocative test that was originally done with barbiturates, amobarbital, primarily, and is presently primarily done with lorazepam.

The person can be given lorazepam 1 to 2 milligrams by slidium. intravenous push are two milligrams intramuscularly and in many persons with catatonia that will essentially result in their awakening from a stupor and being able to interact. It's a fairly dramatic response when the person is responsive. A negative test does not rule out catatonia, but a positive test, meaning the person wakes up and becomes responsive is fairly pathonomonic that this person is suffering from catatonia. Physiologists tend to describe catatonia as an abnormal variant of the fight-flight response. The animal that goes berserk is wildly active.

That's somewhat like excited catatonia. In contrast, the animal that freezes, quotes, plays potting. Possum, maybe an example of catatonic stupor. In their normal state, those serve survival. However, the catatonia occurring in conjunction with medical, neurological, or psychiatric disorders appears to be an aberration or an abnormal presentation of that underlying mechanism. Yeah, two things. One is the benzodiazepine challenge is a lot of fun.

For me, it's really exciting when I have medical students on. I want them to see that catatonic patient before. And then we give the Ativan, ideally, you know, 2 milligrams IV. Sometimes we have to give it IM. And then you watch them, you know, 15 minutes later or so. And it's a huge, it can be a huge change. So things that you should notice before are those subtle, like how many seconds does it take for this person respond? And does that decrease in the time?

And if they have like the echolalia or the echopraxy, it does that change. The other thing is, do they move faster? Do they move more easily? Do they talk more fluidly? And then also the intense fear inside of them, does that decrease where they don't feel so like locked in to this like frozen state? Yeah, when the person responds to the benzodiazepine, it's quite a dramatic response.

It appears almost magical in terms of the person going from this frozen, stuporous state to alert, interactive, relatively normal appearing in terms of motor and speech functions. The reason, of course, for doing this either intravenously or intramuscularly is you're aiming to get a relatively high peak of the medication into the brain, relatively quickly. It's doing it orally often won't tell you anything because the peak plasma concentration isn't either fast enough or high enough. Yeah.

So if it's IV, we reexamine five minutes after, because that's when you're going to get that nice peak. And if it's IM, what would you say, like 15? 15 to 20 minutes after the IM injection. Yeah. And then to your second point of the, this sort of frozen state, you know, we talked about the polyvagal theory in another episode where that myelinated nucleus ambiguous, parasympathetic is that rest and relaxation.

And then you have the sympathetic nervous system, which is the second sort of fight and flight. You know, initially people freeze, look at the surroundings, usually run away, and then when necessary fight. and sometimes people puff up in that in that sort of fight and flight place as well so a lot of posturing and such as normal in the animal kingdom and in the human kingdom and then that third state is the dorsal vagal so it's a different vagus system

and it's that unmyelinated dorsal vagal system which is the parasympathetic shutdown which occurs when someone's in a traumatic situation or if someone's in a very dissociated system situation or, you know, disorganized attachment at one years old, they kind of go into that state for a brief moment, and that's how they get labeled in the disorganized attachment, or in the adult attachment interview, they go into that state for a little bit if they're in the unresolved type of the adult attachment interview.

But interestingly, what we talked about, Dr. Cummings, was that sometimes people get stuck in that in a more chronic state where their brain is kind of stuck there. And I think this is a really helpful way of understanding Catatonia. It's different than borderline personality disorder, which I think they get stuck in kind of that dissociated state as well. But they get kind of, in Catatonia, they get stuck in this state for weeks, for months even. And the progression is as we talked about. So I think that's a really helpful kind of way of thinking about it. Yeah.

Basically, these people, when they are either in an accessible, excited or catatonic stupor, some of them will respond to the benzodiazepine and will wake up nicely or will calm down if it's the excited state. There are, however, a subgroup who don't respond, and indeed in those cases, most often we're then talking about proceeding to electroconvulsive therapy as the next step in treatment. Often a relatively emergent use of electroconvulsive therapy because often by the time they've reached the point where they're no longer responding,

they're often in a more advanced catatonic state. So one thing that you pointed out, I think that is that schizophrenia does not respond as well to the benzodiazepines? that's correct one of the caveats with catatonia is to always remember

that the catatonia is a secondary phenomena associated with an underlying illness and the underlying illness does have a profound influence on both the presentation and the responsiveness of the catatonia

it's important to treat both the catatonic syndrome but also don't forget to treat the underlying illness. And indeed, the schizophrenic patients are less likely than the mood-disordered patients to respond to the benzodiazepine challenge. Same thing is true of some of the neurologic conditions. Some people with encephalitis or with profound metabolic disturbances

may be less likely to respond to the benzodiazepine challenge. and in those cases, of course, you're treating both the underlying medical illness and the catatonia. Yeah. And then another thing I think it's really important to point out is that if they respond to the benzodiazepines, you want to keep increasing the dose until, you know, you get the full response. And you know you've gone too high when they develop lateral nistagmous. And that's something I learned from Dr. Cummings as well. So you want to mention anything about that?

Yeah. And this is true for any of your patients that you treat with benzodiazepine or in the context of other disorders with an anti-epileptic medication. If you're wondering if the person is reaching a point where they have more medication than they should have, a quick and easy clinical test is to do lateral gaze, have them follow your finger as far right and as far left. left as they can, if you start to see nistagmus a beating of the gaze at the end of each of those arcs, they're reaching their threshold for how much of the medication they can tolerate. Having said that, frankly, a lot of people are surprised with how much benzodiazepine it may take initially to keep the catatonia under control. Certainly doses of loresopam, for example, of up to

around 9 to 10 milligrams a day is not unusual. And then often people are switched to clonazepam because of its longer half-life. And indeed, in those cases, the person may require doses of 5 or 6 milligrams a day initially to keep the catatonia under control. Once the underlying illness is treated in the vast majority of patients, it's possible to gradually taper and discontinue the benzodiazepine. You will find a small number of patients who are very prone or vulnerable to catatonia in whom you can get them to a lower dose, but you'll find a threshold below which

the catatonic signs and symptoms reemerge. And for those people, they may wind up needing treatment with chronic benzodiazepine. Yeah, and one thing I think is really important to consider in this management is you can keep in, you know, every four hours, you can give them another two milligrams of that Ativan in that first day. And you can kind of see how much they require. So you can go up pretty quickly on this medication. I see one of the mistakes is they'll start it out like one, three times a day. And then the next day they'll go up to one, four times a day. And I don't think you need to go up that slowly. I don't know if you have your thoughts on that. No, in fact, you want to be relatively aggressive. You want to get the catatonia under control as quickly as you can.

If they are a benzodiazepine responder, then indeed the optimal way to treat them is to give them two milligrams every four hours, go and look at them. If they are staying fluid, active, they're not stuporous, or they're not excited, then at the end of 24 hours, you have a pretty good tally of how much it took to do that, and you can then continue that as their ongoing treatment initially. You may then think about perhaps wanting to switch them to the longer acting claw nasopam, depending on the circumstances.

If they are not a responder, then you're probably looking at pursuing electric convulsive therapy. And in some studies, the remission rate is around 80% with benzodiazepine. So it really is the first line of management. Now that being lower in the patients with schizophrenia, one thing that I think is really helpful to kind of understand is once they get out of the catatonia, you're not just dropping them off of the benzodiazepine quickly. we mentioned going down 0.5 milligrams of the Ativan per month. So if they're on 14 milligrams, the taper may be over the course of a year.

Yes. Yeah, it's a very gradual taper with ongoing monitoring for reemergence of subtle signs and symptoms of the catatonia. You know, if you have somebody who's been catatonic, Every time you do a mental status examination on that person, you should be paying very close attention to how fluidly they move. Are they developing any speech latency? Are there any even breakthrough minor echolalia episodes? Because that will tell you that the catatonia has not fully resolved. In part, that depends on how well the underlying condition.

has responded to treatment as well. Yeah. And let's talk a little bit about ECT, the electroconvulsive therapy. So if you're like a therapist or, you know, a non-medical person listening to this, this is when we're applying a charge, usually to the brain,

we put someone in a paralytic. So they're not, their whole body is not shaking, unlike many movies that you may have seen where people are going through ECT. you know, in the olden days, you know, you would see the whole body shake and, you know, maybe they would hurt their teeth and such. But nowadays, it's fairly well controlled. And it really is miraculous for someone with catatoni who's not responding to Ativan. I mean, it is life-changing,

how quickly it can work. And if it's not effective, even like two to three ECT are usually effective to remove someone from the catatonic state, four to six to prevent recurrence, 10 to 20, maybe needed in resistant cases. What are your thoughts on ECT, Dr. Cummings? Well, and the person who has developed catatonia, again, the end of catatonia, if it is left untreated, is death,

either in the stupor state because they stop eating and drinking, or in the excited state because they keel over and die of cardiovascular collapse. So in those cases who are not benzodiazepine responders, the ECT is literally life-saving. And indeed, the response is often exceedingly rapid. I've seen dramatic changes after the initial treatment. And indeed, usually as the ECT is being completed, then the person is often put on a benzodiazepine,

to which they have become responsive. There are a few other treatments that have been looked at. NMDA receptor antagonists like Amantadine and Mamentine have a small amount of data supporting their use. The anti-epileptic toperimate probably due to its antagonism at metabotropic Glutamate receptors may have some utility, but frankly, the data for these other treatments is very preliminary at this point. The two established treatments are really benzodiazepine and ECT. Yeah, and so ECT, there's so much stigma around ECT, but think about how

transformative it can be. And if you're practicing psychiatrist and you've seen patients who are catatonic and they're not responding to Ativan. It is truly life changing to see someone go through this. And the family is shocked at how well it works most times. I would love to do an episode fully on ECT. I got Dr. Trankelow who wants to do it. Maybe Dr. Cummings can have a couple words as well. But any other things on ECT you want to mention? I would say that these days, as ECT is done, the stigma is undeserved. You know, ECT is essentially a minor medical procedure, usually done in an outpatient setting, outpatient surgery setting, involves putting the person briefly to sleep with a short-acting

barbiturate, as you mentioned, paralysis, usually with succinctil-choline. the person then has the stimulus applied. They have a seizure that lasts for less than a minute, and usually they're up and around in less than a half hour later. Yeah, it's truly amazing. Melancholic depression, also we use ECT, but Catatonia for me is probably the biggest win, and when I really consider it,

even if they're partially responding to Ativan, they can get a full response from the ECT. Okay. I think now what would be really valuable is to go through some of the related things to catatonia and talk about how catatonia is a little bit different. So, for example, NMS, neuroleptic malignant syndrome. When you see a patient with NMS, how do they differ from someone who has catatonia? Okay. Initially, they can look somewhat similar.

Neuroleptic malignant syndrome, as the name suggests, is an adverse response to a dopamine antagonist, usually an antipsychotic, although things like other anti-emetic agents can rarely cause NMS as well. NMS is characterized by autonomic arousal. The person has a rapid heart rate, rapid breathing. they develop fever, often extreme fever, 104 to 108 degrees is not unusual. They will develop febrile seizures, and they exhibit muscle rigidity. Unlike the catatonic person who slows down and may hold a posture, these people are rigid,

and indeed there is associated with that muscle breakdown and elevation of creatine and phosphokinice or cK, often into the tens of thousands in fully evolved neuroleptic malignant syndrome. Yeah. So NMS, severe decrease in central dopamine, dopaminergic activity, usually from a dopamine blocker, You get the tachycardia, hyperthermia, high blood pressure, rigidity. You get the mutism and stupor, but you also get things like increased CPK, and that can lead to acute renal failure and the high fever. The patients who are at risk for developing NMS have had a treatment of neuroleptic drugs,

maybe a history of catatonia, history of schizophrenia, history of mood disorders, especially postpartum depression, history of alcoholism, substance abuse disorders, history of agitation, dehydration, exhaustion, history of basal ganglia disorders, things like Parkinson's, Wilson's disease, honey's disease, tardive dyskinesias, or dystonias, and low serum iron,

especially when neuroleptics are prescribed. Yeah, and usually in terms of the neuroleptics, the most common presentation is in someone who, because they have presented with psychomotor agitation associated with psychosis, they've often received a high potency neuroleptic medication like haloperidol, flufenazine, and they've often have received repeated doses for the purpose of getting their psychomotor agitation under control. In other words, their dopamine blockade. has risen rapidly and their dopamine signaling has correspondingly dropped off rapidly,

resulting in vulnerability to neuroleptic malignant syndrome. Another syndrome that may mimic catatonia initially especially is serotonin syndrome. This is a response to excessive serotonin in the central nervous system can rarely result from very rapid rises in serotonergic antidepressants, the SSRIs, but more commonly occurs if the person has their serotonin increased by more than one mechanism. For example, if you give them a serotonin re-uptake inhibitor, and at the same time the person is given a direct serotonin agonist, like a triptan. or they're given a monoamine oxidase inhibitor that blocks the breakdown, the metabolism of serotonin.

They may develop serotonin syndrome initially characterized by excitement, stupor, nausea, vomiting, diarrhea, confusion, and then ultimately coma. So it diverges from catatonia, but in the very early stage, images, innamess, catatonia, and serotonin syndrome can look somewhat alike. Yeah, and I've seen a number of primary care docs put on TCA's on top of like Symbolta thinking, okay, I'm going to treat this headache or I'm going to treat this, you know, pain issue with this amyptylene. They may get a lot of anticholinergic symptoms, which I've seen, you know, if you have a 2D6 blocker like Prozac and then you stick on amatryptylene, it may increase the level amtryptylene and the anticholinergic and give someone another issue like a delirium.

Yeah, a very dangerous thing to do. The two SSRIs that are very potent 2D6 inhibitors are fluoxetine and paroxetine. All of the tricyclic antidepressants depend on 2D6 for metabolism as their primary route. Of course, the major caveat with the tricyclics is the lethal concentration for the tricyclics is only six to eight times the therapeutic concentration. Yeah. So coming back to serotonin syndrome, I've seen this as well when people try to overdose on SSRIs. They take a ton of SSRIs all at once and then they develop that confusion, anxiety, nausea, vomiting, that sort of ataxia in coordination, restlessness, myoclonus, tremor, hyperreflexia, autonomic abnormalities, so they could be hyper or hypotension,

tachycardia, lots of sweating. And so, of course, the first thing to do is to get them off of the serotonin medications immediately. And benzodiazepines can manage the agitation. Sometimes you do a 5HT receptor antagonist, but that's not considered first line. No. The principle of course is to stop the offending agent or if the person's taken an overdose, you're essentially waiting for it to be catabolized and to decrease. And the mainstay of treatment is really supportive care to keep the person hydrated to treat them usually with intravenous fluid and supports essentially to allow them to recover. One of the other big things to look at when you're looking at a differential is delirium. Delirium is a waxing and waning of attention. So it's a decrease in attention. So they fail things like the serial sevens, you know, countdown by 21 by threes.

Draw on a clock, they usually fail at that. And they can't spell world backwards. delirium has kind of this waxing and waning. So if you get the history, you know, they were pulling out their lines and then they were more sedated. They looked sedated for a while. It's a common medical issue or medical issues commonly lead to delirium in a hospital. There's a high rate of delirium, especially in ICU's. There's different types of delirium, hyperactive, hypoactive mixed. So hyperactive is the is the type of delirium where they're pulling out their lines, they're yelling, they're throwing things, they're seeing visual hallucinations, hypoactive.

Motor retardation, apathy, slowing of speech. And then you can have the mixed hypo and hyperactive. And catatonia and delirium can look pretty similar. And so I think it's worth discussing when we would think this is more catatonian, we want to give Ativan versus when this is more delirium, because Ativan, I don't think is going to help delirium. actually benzodiazepines make delirium worse. And one of my pet peeves is when the ER doc gives the benzodiazepine

and maybe even something like Benadryl to the delirious patient. And we're like, come on, what are you doing? Yeah, indeed. In most deliria, benzodiazepine is contraindicated. The one exception to that is alcohol withdrawal delirium, in which case you may indeed want to very aggressively give the person of benzodiazepine because you're giving a cross-tolerant drug and what's driving the delirium in that case is alcohol withdrawal but that's a very singular case of sedative hypnotic

withdrawal that type of delirium that doesn't account for the majority of delirium in fact delirium most often represents a critical breakdown in brain function related to severe metabolic disturbance of some sort or exposure to anesthesia as a common cause of delirium in hospitals. It's estimated that post-operatively about 40% of people experience a delirium. Fortunately, most of those are transient and short-lived and are essentially the quiet sort of delirium. But if you look for it, it's there. Most people post-op are not entirely clear.

In the other types of delirium, you're really looking for the underlying cause of the delirium. You may need to treat with an antipsychotic, or in some cases, antipaleptics have been used to treat delirium, particularly if it's associated with seizure. And both are reasonable treatment. again, though, with most delirium, what you're really looking for is what is the underlying cause of the delirium? Because that will guide your treatment. Yeah. One thing that I think about with delirium is coming back to like having them draw clock, having them spell world backwards, having them do serial, you know, threes, count down by 21 by threes.

I think that if you suspect at all that someone's delirious, do those things. somebody who's catatonic, they may not move very much, so it may take them a long time to draw the clock. But I don't think they're as confused or they don't have the attention issues as someone with delirium. Do you have any thoughts on that? No, no, usually if, well, provided they haven't reached the point where they don't produce any speech or behavioral response, person with catatonia will give you accurate answers, albeit very slowly. Whereas the person with delirium will not. They'll give you confused answers, except for those few periods when they have what's called a lucid interval.

Again, as you pointed out at the beginning, delirium is characterized by a fluctuating level of consciousness and alertness. Yeah, so when I have my residents who are on C&L, go see someone who's, they think is catatonic. I always have them draw clock, do the serial threes, spell world backwards, tell me how that goes, and then let's go see them. Sometimes in a catatonic patient, they'll have a little bit increased tone when you move their hands, arms, and that'll go away after the Ativan. And then if you give a delirious patient Ativan, they tend to just sleep, whereas the catatonic patient will be, you know, the speech will change, they'll be moving differently.

so that's another sort of clinical pearl. Indeed, in the catatonic stupor, when you give them the benzodiazepine, paradoxically, they quote to wake up and become interactive, whereas in the delirious patient, just as in most of us, if you give them a benzodiazepine, they're likely just to go to sleep.

Yeah. I think it might be worth talking a little bit about what we find in the brain going on. What is going on in the brain? as we kind of alluded to earlier, appears to be an abnormal activation of the fight-flight response. There is a dramatic increase in dopamine signaling, dramatic increase in noradrenergic signaling,

and by comparison of relative deficit in serotonin signaling in the catatonic brain. There also appears to be an increase in glutamaternity. purgic signaling, which is what got people attracted initially to seeing if the glutamate antagonists would have any effect on catatonia. And indeed, they do, albeit the data set is preliminary and small at this point. There's a really nice article from Lancelette, Lancet Psychiatry 2019, the structure and neuromechanisms of catatonia. And they conclude that neuroimaging studies of of patients with the history of catatone indicate poor functional activation of SMA, primary and secondary motor cortices, inferior parietal cortex and basal ganglia during self-initiating movements,

lower cerebral blood flow in the right prefrontal and parietal cortex, and reduced GABA-A receptor density in the left sensor motor cortex. Essentially, these are people in whom there is a failure to appropriately, again, in the stuporous catatonia, a failure to activate both the accessory and primary motor cortices, essentially a failure of the activation signal from the basal ganglia. They also said MRI studies reported that orbital frontal cortex dysfunction, which is partly reversible by, Lurazepam administration. That was interesting to me because they also find that in people with PTSD as they relay their trauma narratives.

There's a decrease functioning in their frontal lobe and the different parts of the brain that sense body sensation. And what we're talking about is a similarity to the dissociative phenomenon or that shutdown, that extreme shutdown. Yeah. Well, it makes sense. these are related pathologies in the sense that some of the same frontal circuits are involved in both conditions. Catatonia being an abnormal activation of the fight fight response and of course PTSD being related to an enduring alteration based on exposure to extreme trauma threat of death or similar threat.

Yeah. So prognosis at this point is pretty good if treatment is given with what treatments we have. Yes, indeed. Response rates to the benzodiazepines, excluding schizophrenia are 80%. Even the schizophrenic patients, though, have at least a better than 50% chance of responding to the benzodiazepines. Almost all catatonic patients will respond to electroconvulsive therapy. as we learn more about the glutamate modulators, we may have additional treatments that we can bring online

to help avoid the development of catatonia. It's one of the pleasant things in psychiatry when you find something that is so rapidly and so well responsive provided, of course, we recognize that the person is developing catatonia. Yeah. So I would conclude that the reason why we spent so much time talking about the history,

talking about the different symptoms, is because the first step is to really identify this group out of the other sick patients that we treat. And some of the subtle signs like that delay in speech, maybe echolalia, a little bit increased tone in the muscles if you just move their arms. And, you know, a history of decreasing weight, maybe not drinking as much.

You know, these are the things that kind of like, raise our suspicion. And I think it's really important to have that suspicion when we're in the inpatient setting or when we're treating patients. And when we get that suspicion, you know, getting a good family history, I think, you know, when I cover the impatient setting on some weekends, I'll see one of these patients. And I'll be like, you know what? That patient has in them a lot of fear.

So my affective empathy, sort of reading of them, is that they seem very fearful but very locked into a frozen state. And from there, you know, my suspicion goes up and I'm like, you know, what might be going on here? Is this the normal picture? Is this the, is this just a depressed patient? And getting that family history, getting on the phone with a family is very important to getting a couple of those key details of, okay, what happened first, what happened next, what happened next? What did, when did they stop talking? When did you notice that?

when did they stop eating? How long has that been going on? When did they start losing weight? Did they stop drinking? What are the other symptoms that you notice? And getting a quick little history like that can be very, very helpful to getting the clinical picture. Yeah, indeed, very much so. And indeed, I always encourage people who are treating patients in addition to psychiatrists talking to their patients. Psychiatrists should not forget that they are physicians. They should examine their patients, do a physical. exam, do a neurological exam, obtain collateral history. People who are vulnerable to catatonia often have had prior episodes. And if you describe what catatonia is to family and friends,

they may well be able to tell you, yes, the last time he was severely ill, that's what happened to him. Yeah, I have a patient who, in getting a close history, it seemed like she had catatonia back when she was, I think about, you know, in her late adolescence. And that was kind of that eye-opener to me like, okay, this sounds like the second episode of this sort of, you know, when she gets really ill, this is what happens. Okay. Dr. Cummings, any other things that you want to mention about this before we wrap it up? I think the one thing I would say in closing is just to encourage people to maintain a high index of suspicion for catatonia. When you're doing your mental, many mental state examination, indeed, pay attention to how well the person moves.

Do they have speech latency? You know, those are the very earliest things that you will see and somebody who is headed toward catatonic stupor. All right. Well, Dr. Cummins, thank you so much for coming on. We will have copious notes from this episode, even more things that we didn't even get to discuss. I think are important. We'll put those in the resource library. You can follow that from psychiatrypodcast.com,

free resources or from the show notes. We have a link to that page. And it's so fantastic to have you on, Dr. Cummings. Thank you so much for your time. I know there's a lot of gratitude out there from people who are getting to listen to this. And I really appreciate you for that. Oh, well, thank you.

I enjoyed it. All right. We'll leave it there.