Gavanshir

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Early 30s patient with hx of bipolar disorder who was brought in by police because she was reported missing by her family. I admitted her a few days ago and at that point she was conversant, well-groomed, not manic or psychotic and denying/minimizing everything. She was however incontinent on multiple occasions from CPEP to her room.

Now since admission, she has been mute and not eating/drinking for the last 48 hours. She has been laying in bed since yesterday and prior to that she had been sitting in a chair for pretty much the entire day in the dark. I just did a quick physical. She clearly had eye movements but wouldn't open her eyes to command or to passive retraction of her eyelids. She seemed to be actively resisting the retraction of her eyelids.

Otherwise, her vitals are stable, DTRs in upper and lower limbs are present. No cogwheel rigidity. She does have some slight voluntary movement of her limbs, e.g. she moved her arm while I was doing passive leg movements. Reacts to pain and grimaces. Her labs were generally fine, just a slightly elevated white count and her anion gap is slightly elevated too. Getting repeat labs today.

Is there a better way to tease out intentional refusal to interact with the world and to eat/drink vs signs of catatonia? Can incontinence and resistance to eyelid retraction in any way associated with catatonia or should I worry about something else?
 

clausewitz2

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Have you done a Bush-Francis or some similar scale on her? I just read a French case series arguing that incontinence I'd an underappreciated sign of catatonia, at least in adolescents. I would be tempted to do a proper Ativan challenge and see what happens.
 
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Gavanshir

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Yes I did, not sure how to interpret though. Three signs are present for items 1-14 and total score is 8 or maybe 9.

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HarryMTieboutMD

What has her behavior been like on the floor since initial admission (ie, was this transition abrupt... any objective signs in the interim of mania or depression?). Your main differential is going to be depression with significant psychomotor ******ation and avolition (which is NOT catatonia if catatonic criteria are not met). Also, I think Kraepelin was right in viewing Catatonia as end stage psychosis, but he was wrong in attributing it solely as a state of the Dementia Praecox (when he incidentally clearly describes patients we would now call catatonic as mixed states in the Manic Depressive Insanity). Nevertheless, people do not become so psychomotor ******ed depressed that they become catatonic... there has to be a psychotic component

I like the BFCRS, but ultimately Catatonia is a clinical judgment. Like any psychiatric diagnosis, the symptoms can be varied and extend far beyond the DSM, but the current criteria are *reasonably* well validated. THINK THROUGH THE CRITERIA Make sure you do your motoric exam correctly (when assessing waxy flexibility or catalepsy you have to instruct the patient that they are not obligated to leave their limb in the position you move it, etc). Fish's psychopathology/Fish's schizophrenia have good instructions on this. Though not part of the criteria, I like to look for gegenhalten, mitgehen, and mitmachen.

Contrary to dogma in psychiatry, the evidence for Benzos in catatonia is REALLY weak (read the 2008 Cochrane review on this). A PARENTERAL ativan challenge (at a low dose, don't increase it to 7mg TID like uptodate says to do) is ok for diagnosis and to get the patient moving to prevent DVTs but often not sustainable as treatment. The evidence is better for ECT and antipsychotics. Contrary to what Max Fink says, you will probably NOT throw your patient into NMS if you give him or her antipsychotics (this is based on really weak evidence as well).
 

clausewitz2

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What has her behavior been like on the floor since initial admission (ie, was this transition abrupt... any objective signs in the interim of mania or depression?). Your main differential is going to be depression with significant psychomotor ******ation and avolition (which is NOT catatonia if catatonic criteria are not met). Also, I think Kraepelin was right in viewing Catatonia as end stage psychosis, but he was wrong in attributing it solely as a state of the Dementia Praecox (when he incidentally clearly describes patients we would now call catatonic as mixed states in the Manic Depressive Insanity). Nevertheless, people do not become so psychomotor ******ed depressed that they become catatonic... there has to be a psychotic component

I like the BFCRS, but ultimately Catatonia is a clinical judgment. Like any psychiatric diagnosis, the symptoms can be varied and extend far beyond the DSM, but the current criteria are *reasonably* well validated. THINK THROUGH THE CRITERIA Make sure you do your motoric exam correctly (when assessing waxy flexibility or catalepsy you have to instruct the patient that they are not obligated to leave their limb in the position you move it, etc). Fish's psychopathology/Fish's schizophrenia have good instructions on this. Though not part of the criteria, I like to look for gegenhalten, mitgehen, and mitmachen.

Contrary to dogma in psychiatry, the evidence for Benzos in catatonia is REALLY weak (read the 2008 Cochrane review on this). A PARENTERAL ativan challenge (at a low dose, don't increase it to 7mg TID like uptodate says to do) is ok for diagnosis and to get the patient moving to prevent DVTs but often not sustainable as treatment. The evidence is better for ECT and antipsychotics. Contrary to what Max Fink says, you will probably NOT throw your patient into NMS if you give him or her antipsychotics (this is based on really weak evidence as well).

Do you have a reference for the efficacy of antipsychotics for catatonia? I am having difficulty finding recent papers supporting this idea, but finding a lot of papers suggesting you should hold dopamine antagonists generally.
 

Merovinge

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What has her behavior been like on the floor since initial admission (ie, was this transition abrupt... any objective signs in the interim of mania or depression?). Your main differential is going to be depression with significant psychomotor ******ation and avolition (which is NOT catatonia if catatonic criteria are not met). Also, I think Kraepelin was right in viewing Catatonia as end stage psychosis, but he was wrong in attributing it solely as a state of the Dementia Praecox (when he incidentally clearly describes patients we would now call catatonic as mixed states in the Manic Depressive Insanity). Nevertheless, people do not become so psychomotor ******ed depressed that they become catatonic... there has to be a psychotic component

I like the BFCRS, but ultimately Catatonia is a clinical judgment. Like any psychiatric diagnosis, the symptoms can be varied and extend far beyond the DSM, but the current criteria are *reasonably* well validated. THINK THROUGH THE CRITERIA Make sure you do your motoric exam correctly (when assessing waxy flexibility or catalepsy you have to instruct the patient that they are not obligated to leave their limb in the position you move it, etc). Fish's psychopathology/Fish's schizophrenia have good instructions on this. Though not part of the criteria, I like to look for gegenhalten, mitgehen, and mitmachen.

Contrary to dogma in psychiatry, the evidence for Benzos in catatonia is REALLY weak (read the 2008 Cochrane review on this). A PARENTERAL ativan challenge (at a low dose, don't increase it to 7mg TID like uptodate says to do) is ok for diagnosis and to get the patient moving to prevent DVTs but often not sustainable as treatment. The evidence is better for ECT and antipsychotics. Contrary to what Max Fink says, you will probably NOT throw your patient into NMS if you give him or her antipsychotics (this is based on really weak evidence as well).
You clearly have good experience on the subject, but using atypicals to treat catatonia has NOT been good from my time in neuropsychiatry. We have seen several cases of malignant catatonia and NMS that appear to be the result of agitated catatonia + Haldol IM; 1 in particular in a young pregnant lady that required about 6 months of inpatient hospitalization through her delivery before mental status resolved (those kind of cases you'll never forget). I have absolutely seen a number of patients get better with BZD tx, most in a relatively dramatic manner. I have absolutely seen folks with Bipolar I have catatonic episodes w/o marked psychotic features that did improve with BZD's although of course you should be treating the underlying mood d/o as well.

I definitely agree that this agree of psychiatry could really stand to have better research, particularly given the serious consequences of improper management.

Also, given your BFCRS above and known Bipolar diagnosis, case does sound like probable catatonia to me and definitely warrants an Ativan challenge.
 

NickNaylor

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You clearly have good experience on the subject, but using atypicals to treat catatonia has NOT been good from my time in neuropsychiatry. We have seen several cases of malignant catatonia and NMS that appear to be the result of agitated catatonia + Haldol IM; 1 in particular in a young pregnant lady that required about 6 months of inpatient hospitalization through her delivery before mental status resolved (those kind of cases you'll never forget). I have absolutely seen a number of patients get better with BZD tx, most in a relatively dramatic manner. I have absolutely seen folks with Bipolar I have catatonic episodes w/o marked psychotic features that did improve with BZD's although of course you should be treating the underlying mood d/o as well.
Completely agree - if someone has catatonia, the treatment is not antipsychotics. Not only do they not work but they can make things worse. I've seen a few older patients that started to develop catatonic features even at low doses of antipsychotic (e.g., haloperidol 2 mg BID) with no previous history of catatonia that we were aware of.
 

Blitz2006

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You clearly have good experience on the subject, but using atypicals to treat catatonia has NOT been good from my time in neuropsychiatry. We have seen several cases of malignant catatonia and NMS that appear to be the result of agitated catatonia + Haldol IM; 1 in particular in a young pregnant lady that required about 6 months of inpatient hospitalization through her delivery before mental status resolved (those kind of cases you'll never forget). I have absolutely seen a number of patients get better with BZD tx, most in a relatively dramatic manner. I have absolutely seen folks with Bipolar I have catatonic episodes w/o marked psychotic features that did improve with BZD's although of course you should be treating the underlying mood d/o as well.

I definitely agree that this agree of psychiatry could really stand to have better research, particularly given the serious consequences of improper management.

Also, given your BFCRS above and known Bipolar diagnosis, case does sound like probable catatonia to me and definitely warrants an Ativan challenge.
What dose of Ativan should we give? IM 2 mg PRN until there is a response?

Slightly unrelated question, are BZDs safe in pregnant women?
 

splik

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Slightly unrelated question, are BZDs safe in pregnant women?
for catatonia benzos are safe in pregnancy (as benefits outweigh risks), I would not use if not manic/catatonic/epileptic etc. There is a small risk of cleft palate if used in the first trimester. Later in pregnancy there is a risk of floppy baby syndrome in the neonate, apneic episodes, problems with sucking etc. But in general they are safe
 

splik

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What has her behavior been like on the floor since initial admission (ie, was this transition abrupt... any objective signs in the interim of mania or depression?). Your main differential is going to be depression with significant psychomotor ******ation and avolition (which is NOT catatonia if catatonic criteria are not met). Also, I think Kraepelin was right in viewing Catatonia as end stage psychosis, but he was wrong in attributing it solely as a state of the Dementia Praecox (when he incidentally clearly describes patients we would now call catatonic as mixed states in the Manic Depressive Insanity). Nevertheless, people do not become so psychomotor ******ed depressed that they become catatonic... there has to be a psychotic component

I like the BFCRS, but ultimately Catatonia is a clinical judgment. Like any psychiatric diagnosis, the symptoms can be varied and extend far beyond the DSM, but the current criteria are *reasonably* well validated. THINK THROUGH THE CRITERIA Make sure you do your motoric exam correctly (when assessing waxy flexibility or catalepsy you have to instruct the patient that they are not obligated to leave their limb in the position you move it, etc). Fish's psychopathology/Fish's schizophrenia have good instructions on this. Though not part of the criteria, I like to look for gegenhalten, mitgehen, and mitmachen.

Contrary to dogma in psychiatry, the evidence for Benzos in catatonia is REALLY weak (read the 2008 Cochrane review on this). A PARENTERAL ativan challenge (at a low dose, don't increase it to 7mg TID like uptodate says to do) is ok for diagnosis and to get the patient moving to prevent DVTs but often not sustainable as treatment. The evidence is better for ECT and antipsychotics. Contrary to what Max Fink says, you will probably NOT throw your patient into NMS if you give him or her antipsychotics (this is based on really weak evidence as well).
Normally your posts are great but there is so much garbage in this post I don't know what you were thinking

1. catatonia is NOT simply and end-point of psychosis and can result from a range of non-psychotic diagnoses (manic-depressive illness, melancholia and autism being the big 3). Yes you may see psychosis but it is wrong to conflate psychosis and catatonia unless it is clear that the catatonia is a response to psychosis (for example a delusion that the world will collapse if the patient moves).
2. I wouldn't pay much attention to Kraepelin here, he got it wrong as he did with so many other things. Kahlbaum hit the nail on the head when he connected the "tension insanity" to affective disturbance. No psychosis is required for catatonia to emerge
3. You can of course see catatonia in organic disease - I have seen catatonic features in limbic encephalitis, CJD, and bvFTD
4. whether there is a difference between depressive stupor and melancholia with catatonic features is a point of contention. but yes, you can be so depressed that you become catatonic
5. autism and intellectual disability commonly are associated with catatonia in people without any evidence of psychosis
6. periodic catatonia is another diagnosis that I do not think it is accurate to characterize as a psychotic disorder (as there are no psychotic symptoms) and often responds marvellously to benzos and neuroleptics are not indicated
7. I think it is disingenous to throw in a cochrane review to trash benzos. Of course there is no good trial data on catatonia, these patients cannot usually consent to participate in RCTs! The fact is, you do not need an RCT to show you whether something works when the results are so blindingly obvious as they are in catatonia with benzos (mania's response to lithium was another finding that did not need an RCT so striking were the results, though Cade's 1949 study was nevertheless followed up by a 1954 controlled trial by Schou)
8. The one thing I would agree with is that benzos don't always work. ECT is by far and away the most effective treatment, but even ECT does not always work
9. I would also agree the evidence of harm from antipsychotics is sometimes overstated, but I would in generally strongly discourage the use of conventional neuroleptics, and be cautious about atypical neuroleptics. Patients can and do develop NMS particularly in the malignant form of catatonia, when given neuroleptics, particularly haloperidol. Again, of course the "evidence-base" is weak because you cannot ethically study this due to lack of informed consent and the question of the very real potential for harm. In some cases it is certainly appropriate to institute neuroleptics, particularly as the catatonia begins to clear
10. hysteria and PTSD are other diagnoses where a catatonia syndrome can occur. of course it is somewhat debatable whether this represents a true catatonia syndrome, or not
11. if you don't ramp up the benzos to as high as tolerated when not seeing an effect, you are going to miss the effect. Yes, sometimes you need to be giving 7mg tid or higher to patients in order to see an effect. often using oral lorazepam can work fine, parenteral is only needed if you can't get the pt to take it orally. We are also underutilizing barbiturates imho, which is what they used in the past, and may be appropriate for more refractory cases
 
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HarryMTieboutMD

Do you have a reference for the efficacy of antipsychotics for catatonia? I am having difficulty finding recent papers supporting this idea, but finding a lot of papers suggesting you should hold dopamine antagonists generally.
You clearly have good experience on the subject, but using atypicals to treat catatonia has NOT been good from my time in neuropsychiatry. We have seen several cases of malignant catatonia and NMS that appear to be the result of agitated catatonia + Haldol IM; 1 in particular in a young pregnant lady that required about 6 months of inpatient hospitalization through her delivery before mental status resolved (those kind of cases you'll never forget). I have absolutely seen a number of patients get better with BZD tx, most in a relatively dramatic manner. I have absolutely seen folks with Bipolar I have catatonic episodes w/o marked psychotic features that did improve with BZD's although of course you should be treating the underlying mood d/o as well.

I definitely agree that this agree of psychiatry could really stand to have better research, particularly given the serious consequences of improper management.

Also, given your BFCRS above and known Bipolar diagnosis, case does sound like probable catatonia to me and definitely warrants an Ativan challenge.
This is the only RCT on the subject, even with a small N it is reasonably well done: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2951534/

Again, the first key is diagnosis- I have seen plenty of well intentioned psychiatrists misdiagnose catatonia\ RE Benzos- yes, I've added on PO benzos too (more to treat myself when I was a 'tern) in Bipolar/SCZ patients with catatonic features and have seen them get better as well but absent any good data to back this up, it introduces multiple levels of bias. Again, the case series out there are hardly convincing enough to warrant holding antipsychotics on a catatonic patient.

Yes, malignant catatonia and NMS look very similar, but to say that antipsychotics will throw a catatonic patient into NMS because somehow they are pathophysiologically similar is complete fallacy. I was involved in the case of a Bipolar patient who was getting ECT who became catatonic, but we didn't attribute it to the ECT (which was incidentally stopped because she became delirious, which was temporally and symptomatically separate from the catatonia)- it was the natural course of her illness, receiving an accepted, evidenced based treatment for acute mania notwithstanding. I just haven't seen anything in the literature strong enough to parse worsening catatonia that becomes malignant catatonia despite treatment from NMS by chance from low dose neuroleptics (which happens) from some vague interaction between the catatonic state and antipsychotics.
 
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HarryMTieboutMD

Completely agree - if someone has catatonia, the treatment is not antipsychotics. Not only do they not work but they can make things worse. I've seen a few older patients that started to develop catatonic features even at low doses of antipsychotic (e.g., haloperidol 2 mg BID) with no previous history of catatonia that we were aware of.
No, they are becoming parkinsonian even with low dose antipsychotics. This sometimes can be difficult to parse from catatonia. A lot of the early case reports on NMS described this exactly- a psychotic patient was given antipsychotics, then thought to become catatonic (when in reality they just had >80% D2R blockade) and was given more antipsychotics throwing him or her into NMS (think of end stage parkinsonism where hypothalamic regulation is lost...). Here is a great one from Danny Weinberger in his days as a resident: http://www.ncbi.nlm.nih.gov/pubmed/?term=weinberger+DR+neroleptic+malignant+syndrome
 

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I'd back up and broaden your ddx. I'd make sure you're including delirium in there. Not enough background know to tease out if she has a reason to refuse treatment (doesn't like psychiatry, doesn't accept diagnosis). Further, catatonia can be a symptom of mania as much as psychosis -- the reel is going so fast nothing comes out. So I'd agree with the ativan challenge. Your indication of overusing is if she gets tired/sleepy - then back off.
 

Merovinge

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Normally your posts are great but there is so much garbage in this post I don't know what you were thinking

1. catatonia is NOT simply and end-point of psychosis and can result from a range of non-psychotic diagnoses (manic-depressive illness, melancholia and autism being the big 3). Yes you may see psychosis but it is wrong to conflate psychosis and catatonia unless it is clear that the catatonia is a response to psychosis (for example a delusion that the world will collapse if the patient moves).
2. I wouldn't pay much attention to Kraepelin here, he got it wrong as he did with so many other things. Kahlbaum hit the nail on the head when he connected the "tension insanity" to affective disturbance. No psychosis is required for catatonia to emerge
3. You can of course see catatonia in organic disease - I have seen catatonic features in limbic encephalitis, CJD, and bvFTD
4. whether there is a difference between depressive stupor and melancholia with catatonic features is a point of contention. but yes, you can be so depressed that you become catatonic
5. autism and intellectual disability commonly are associated with catatonia in people without any evidence of psychosis
6. periodic catatonia is another diagnosis that I do not think it is accurate to characterize as a psychotic disorder (as there are no psychotic symptoms) and often responds marvellously to benzos and neuroleptics are not indicated
7. I think it is disingenous to throw in a cochrane review to trash benzos. Of course there is no good trial data on catatonia, these patients cannot usually consent to participate in RCTs! The fact is, you do not need an RCT to show you whether something works when the results are so blindingly obvious as they are in catatonia with benzos (mania's response to lithium was another finding that did not need an RCT so striking were the results, though Cade's 1949 study was nevertheless followed up by a 1954 controlled trial by Schou)
8. The one thing I would agree with is that benzos don't always work. ECT is by far and away the most effective treatment, but even ECT does not always work
9. I would also agree the evidence of harm from antipsychotics is sometimes overstated, but I would in generally strongly discourage the use of conventional neuroleptics, and be cautious about atypical neuroleptics. Patients can and do develop NMS particularly in the malignant form of catatonia, when given neuroleptics, particularly haloperidol. Again, of course the "evidence-base" is weak because you cannot ethically study this due to lack of informed consent and the question of the very real potential for harm. In some cases it is certainly appropriate to institute neuroleptics, particularly as the catatonia begins to clear
10. hysteria and PTSD are other diagnoses where a catatonia syndrome can occur. of course it is somewhat debatable whether this represents a true catatonia syndrome, or not
11. if you don't ramp up the benzos to as high as tolerated when not seeing an effect, you are going to miss the effect. Yes, sometimes you need to be giving 7mg tid or higher to patients in order to see an effect. often using oral lorazepam can work fine, parenteral is only needed if you can't get the pt to take it orally. We are also underutilizing barbiturates imho, which is what they used in the past, and may be appropriate for more refractory cases
Great post! We have had folks on 20mg of Ativan as well for sustained (>1 week) periods of time. It was a bit hilarious when a new pharmacist would come on service, we would know like clockwork because they would call freaked out. The difference can be as strikingly clear as an anesthesic, particularly when withdrawing the BZD.
 

psychattending

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In general I am in agreement with this post from HarryMTieboutMD. For the most part I have found that catatonia tends to be a reflection of psychosis (like Kraeplin says), especially if one does a good exam and history. Yes, one can always find/point out exceptions to the rule (and yes there are organic causes). One of the problems has always been trying to distinguish catatonia from a psychomotor ******ed depression or excessive D2 blockade. DSM-5 tries to help with that by altering the number of signs that have to be present.

Kraeplin was probably wrong with his position that catatonia=schizophrenia (as some studies now indicate [see Adams and Taylor below] and DSM allows). A careful (and painful) reading of his book indicates that 1) 47% of his catatonics had a depressive episode initially, 2)⅓ showed considerable improvement sometimes resembling a complete recovery (remember this is the pre-treatment era). Improvements lasted 2-3 years typically but in one case it was 29 years. The patients always relapsed and developed "dementia" and why he called them dementia praecox. Thus my interpretation of his data is that if he had had antipsychotics, a lot of his patients with dementia praecox might have been given a diagnosis of a psychotic affective illness (or schizoaffective disorder).

Kahlbaum's description of catatonia was really not that different from Kraeplin except Kahlbaum focused on the motor signs. He saw catatonia as a phase in an illness that included depression, mania, and psychosis. Thus, both authors describe catatonia as having motor, psychotic, depressive, and manic type phenomena during the course of their illness. Kahlbaum just saw motor as the core while Kraeplin saw psychosis as the core issue.

In a study by Adams and Taylor (1976) looking at patients with one or more signs of catatonia, 7% had schizophrenia, 62% mania, 9% "endogenous depression", 16% coarse brain disease, and 5% reactive psychosis.

While treatment response studies are pretty sparse and poor, what we have suggests that
1) response rates to benzos is a lot poorer than the "word" on the street. Narayanaswamy et al in 2012 suggested that the response rate to ativan 3-6 mg/d x 3days was down around 33%
2) Peralta et al in 2010 showed that antipsychotics (haldol, risperidone, olanzapine) had a roughly 80% response rate (this was in psychotic catatonics who really did not have much in the way of affective symptoms)
3) Response rate with ECT is probably as high as or slightly higher than antipsychotics. Rohland et al in 1993 in a series of 28 cases found that affective patients (MDD, BD) had a 96% resolution of catatonic signs, whereas catatonic schizophrenics had a 71% response.
4) England et al (2011) in their retrospective review found that benzos definitely helped in only about 28% of cases (they used up to 16 mg/day). ECT worked in 83% of the time when it was tried and antipsychotics worked 86%.

The main problem with antipsychotics is that if the dose is too high they can produce EPS and this is likely what causes some people to conclude that it can worsen catatonia. The best study looking at this is a Peralta and Cuesta 2010 study. They were able to disentangle catatonic signs from parkinsonism. They showed that catatonia improved and the parkinsonism worsened. Haldol was worse but it was given at a higher D2 dose than the other antipsychotics.
 
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psychattending

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Early 30s patient with hx of bipolar disorder who was brought in by police because she was reported missing by her family. I admitted her a few days ago and at that point she was conversant, well-groomed, not manic or psychotic and denying/minimizing everything. She was however incontinent on multiple occasions from CPEP to her room.

Now since admission, she has been mute and not eating/drinking for the last 48 hours. She has been laying in bed since yesterday and prior to that she had been sitting in a chair for pretty much the entire day in the dark. I just did a quick physical. She clearly had eye movements but wouldn't open her eyes to command or to passive retraction of her eyelids. She seemed to be actively resisting the retraction of her eyelids.

Otherwise, her vitals are stable, DTRs in upper and lower limbs are present. No cogwheel rigidity. She does have some slight voluntary movement of her limbs, e.g. she moved her arm while I was doing passive leg movements. Reacts to pain and grimaces. Her labs were generally fine, just a slightly elevated white count and her anion gap is slightly elevated too. Getting repeat labs today.

Is there a better way to tease out intentional refusal to interact with the world and to eat/drink vs signs of catatonia? Can incontinence and resistance to eyelid retraction in any way associated with catatonia or should I worry about something else?
There was a study by Peralta and Cuesta in 2001 in Schizophrenia Research that looked at some of the different signs of catatonia to see how best to define the syndrome. They found that catatonics always had at least 3 signs and non catatonics always had <4 (two non-catatonics had 3 signs). Cutoffs at 3 or 4 had good ROCs and informed somewhat the changes to DSM-5. That paper would list the signs they looked at.
 
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