Ativan for catatonia

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nexus73

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What is the maximum daily dose of ativan you have used for treatment of catatonia? I currently have an inpatient responding to 4 mg QID, with catatonia 2/2 depressive illness. He persists with residual catatonic symptoms, word finding difficulties, latent responses, at times appearing to get locked up in his thoughts when asked a questions. Not sedated at all from this dose.

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Can't you dose a benzo until the patient can't stand up anymore? Before that, you won't cause respiratory depression, right?
 
That's seems to be much higher dose of Ativan that I have seen for Catalonia treatment. I would think if partially responding to Ativan, go for ECT. How long has your pt been on this dose?
 
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What is the maximum daily dose of ativan you have used for treatment of catatonia? I currently have an inpatient responding to 4 mg QID, with catatonia 2/2 depressive illness. He persists with residual catatonic symptoms, word finding difficulties, latent responses, at times appearing to get locked up in his thoughts when asked a questions. Not sedated at all from this dose.

Is it IV or PO?
 
If you're nearing 10mg, I'd say you've saturated the receptors and need to reconsider the diagnosis and/or treatment.
 
If you're nearing 10mg, I'd say you've saturated the receptors and need to reconsider the diagnosis and/or treatment.

I'd respectfully disagree. Depending on the severity and time span of the illness/treatment, I have seen multiple responses far above ten. Our neuropsychiatrists would probably have a patient ever 2-3 months requiring 16-24mg daily (24mg/day is the highest I have gone). The patient who was on 24mg a day badly needed ECT but family was vehemently opposed. When she was trialed on even slightly lower doses of benzodiazapines her catatonia came roaring back. She was minimally sedated on the 24mg but did eventually get off completely after she finally get ECT months later.
 
The dosing is PO, and the patient is not sedated at all with this dose. ECT is being pursued but there is limited availability and will likely need to d/c to SNF and get into it as an outpatient.
 
ECT is if course the answer, but aside from that I'm in the camp of you not failing benzos until you've titrated to the point where side effects are intolerable.
 
NO. Increasing benzos is inappropriate, fruitless, and sometimes dangerous. It is largely dogma driven by people like Max Fink without much data behind it.

First, make sure you are accurate in your diagnosis- understand the phenomenology and clinical context. Also make sure that the patient is not just Parkinsonian/akithetic (this is a bush league mistake that lots of weak-minded people make)
Benzos do work, but only about 30% of the time: https://www.ncbi.nlm.nih.gov/pubmed/22387048

If Benzos don't work, antipsychotics are the next step, with upwards of 80% response rate> Peralta and Cuesta who are among the clearest thinkers in diagnostic psychiatry have shown strong effect sizes, parsing out catatonia from neuroleptic induced movement disorders with clear diagnostic precision https://www.ncbi.nlm.nih.gov/pubmed/20071147

Antipsychotics DO NOT throw catatonic people into NMS. This is an unproven fallacy that max fink has been perpetuating with again little good evidece

ECT has a typically powerful response rate, 70-90% cited various places in the literature and would be my go to for catatonic stupor does not remit to medications.

Bottom line- you can do a benzo challenge if you want, but antipsychotics and ECT are going to work much better.
 
For those interested and not intimidated by Harry's accusations that it is dogma and weak thinking behind the use of benzos, we had this discussion not long ago: https://forums.studentdoctor.net/threads/are-these-less-common-signs-of-catatonia.1222987/

Benzos do work, but only about 30% of the time: https://www.ncbi.nlm.nih.gov/pubmed/22387048
Assuming this is the same study (I'm on my phone and at a party so I'm not reading carefully enough): https://www.ncbi.nlm.nih.gov/pubmed/20804808 then 32 responded to benzos but 68 improved. Out of just 99 subjects. With up to only 6mg of Ativan daily.
 
For those interested and not intimidated by Harry's accusations that it is dogma and weak thinking behind the use of benzos, we had this discussion not long ago: https://forums.studentdoctor.net/threads/are-these-less-common-signs-of-catatonia.1222987/


Assuming this is the same study (I'm on my phone and at a party so I'm not reading carefully enough): https://www.ncbi.nlm.nih.gov/pubmed/20804808 then 32 responded to benzos but 68 improved. Out of just 99 subjects. With up to only 6mg of Ativan daily.

Yeah, I am on a slow call night so I can read a little more carefully. The study that Harry quoted, when compared to the study you cited which is clearly the same cohort, does say that only 32 out of 99 were responders to benzos. What that appears to mean is that only 32 out of 99 showed COMPLETE resolution of symptoms, but that 68 showed improvement in symptoms. This is a very different picture then the quote paints. In fact, the same authors themselves conclude the study you are citing by advocating strongly for the use of lorazepam in these contexts.

Also, the Peralta et al. paper was very careful to only examine neuroleptic-naive psychotic patients without any kind of mood disorder. So I would be very hesitant to go ahead and apply this thinking to your super depressed dude who has developed Cotard's delusion and is now increasingly catatonic. The authors themselves actually state: "... the extent to which both catatonia mechanisms and response to antipsychotic drugs operate across schizophrenia and affective psychoses would require careful, controlled studies that do not exist to date."

I get that Harry feels very strongly about this so I am sure he is not going to stop telling us we are dumb for not throwing neuroleptics at people who are catatonic, but the evidence he is citing is somewhat more nuanced than he is making it out to be.
 
Yeah, I am on a slow call night so I can read a little more carefully. The study that Harry quoted, when compared to the study you cited which is clearly the same cohort, does say that only 32 out of 99 were responders to benzos. What that appears to mean is that only 32 out of 99 showed COMPLETE resolution of symptoms, but that 68 showed improvement in symptoms. This is a very different picture then the quote paints. In fact, the same authors themselves conclude the study you are citing by advocating strongly for the use of lorazepam in these contexts.

Also, the Peralta et al. paper was very careful to only examine neuroleptic-naive psychotic patients without any kind of mood disorder. So I would be very hesitant to go ahead and apply this thinking to your super depressed dude who has developed Cotard's delusion and is now increasingly catatonic. The authors themselves actually state: "... the extent to which both catatonia mechanisms and response to antipsychotic drugs operate across schizophrenia and affective psychoses would require careful, controlled studies that do not exist to date."

I get that Harry feels very strongly about this so I am sure he is not going to stop telling us we are dumb for not throwing neuroleptics at people who are catatonic, but the evidence he is citing is somewhat more nuanced than he is making it out to be.

*sigh*
1) RE Benzos and 30% response rate (which has been shown elsewhere as well with higher doses https://www.ncbi.nlm.nih.gov/pubmed/21677256), thats the entire point. In the Narayanaswamy papers, 1/3 of the patients recovered and were back to baseline (or not catatonic), and the other 60something percent needed ECT. In the England study 60something percent "likely benefitted" this is vaguely defined. Also, England et al note 6/7 patients responded well to Clozapine with more detrimental effects as the drug becomes more "typical", but they do not parse catatonic signs from EPS, etc (and do not describe dosing).

2) Yes, Peralta and Cuesta do discuss limitations with extension to mood disorders; however this was a DSM IV era paper in which catatonia was held in a very Kraepelinian light as a subtype of schziophrenia, and the criteria were not as refined (because the symptoms were in clusters in which only 2 were required), and catatonic features with mood disorders were likewise the same. However, previous work by Peralta/Cuesta and Adams/Taylor hints that catatonia in a diagnostic sense can be extended reliably across schizophrenia spectrum and affective disorders (and peralta/cuesta included both affective and non affective psychotic patients in work they did previously), but 3-4 signs are needed to differentiate it from similar syndromes (psychomotorically ******ed depression, etc)

3) Bear in mind that Kalbaum described catatonia as mostly motoric disorder with periods of "mania" and "melancholia", which Kraepelin concluded were actually "excitement" and "stupor", and that the syndrome itself was a manifestation of the dementia praecox because they all, despite some having periods of recovery, had an unfavorable terminal state. Also, Kraepelin notes that ~50% of his catatonics presented as "depressed", which today, in the area of psychopharmacology and without knowing the terminal state until it happens, might have resulted in a diagnosis of a primary affective disorder. Oddly enough, in the Manic Depressive Insanity Kraepelin clearly describes patients today who we would describe as catatonic, but he doesn't use the term likely because he saw enough patients with the Dementia Praecox that had consistent courses and terminal states. Either way, Kraepelin clear describes the symptoms of catatonia as an "end stage" of psychosis (NOT that some patients become so psychomotorically slowed that they are now catatonic- see peralta/cuesta 2001) as occurring in either primary psychotic or affective disorders.
 
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*sigh*
1) RE Benzos and 30% response rate (which has been shown elsewhere as well with higher doses https://www.ncbi.nlm.nih.gov/pubmed/21677256), thats the entire point. In the Narayanaswamy papers, 1/3 of the patients recovered and were back to baseline (or not catatonic), and the other 60something percent needed ECT. In the England study 60something percent "likely benefitted" this is vaguely defined. Also, England et al note 6/7 patients responded well to Clozapine with more detrimental effects as the drug becomes more "typical", but they do not parse catatonic signs from EPS, etc (and do not describe dosing).

2) Yes, Peralta and Cuesta do discuss limitations with extension to mood disorders; however this was a DSM IV era paper in which catatonia was held in a very Kraepelinian light as a subtype of schziophrenia, and the criteria were not as refined (because the symptoms were in clusters in which only 2 were required), and catatonic features with mood disorders were likewise the same. However, previous work by Peralta/Cuesta and Adams/Taylor hints that catatonia in a diagnostic sense can be extended reliably across schizophrenia spectrum and affective disorders (and peralta/cuesta included both affective and non affective psychotic patients in work they did previously), but 3-4 signs are needed to differentiate it from similar syndromes (psychomotorically ******ed depression, etc)

3) Bear in mind that Kalbaum described catatonia as mostly motoric disorder with periods of "mania" and "melancholia", which Kraepelin concluded were actually "excitement" and "stupor", and that the syndrome itself was a manifestation of the dementia praecox because they all, despite some having periods of recovery, had an unfavorable terminal state. Also, Kraepelin notes that ~50% of his catatonics presented as "depressed", which today, in the area of psychopharmacology and without knowing the terminal state until it happens, might have resulted in a diagnosis of a primary affective disorder. Oddly enough, in the Manic Depressive Insanity Kraepelin clearly describes patients today who we would describe as catatonic, but he doesn't use the term likely because he saw enough patients with the Dementia Praecox that had consistent courses and terminal states. Either way, Kraepelin clear describes the symptoms of catatonia as an "end stage" of psychosis (NOT that some patients become so psychomotorically slowed that they are now catatonic- see peralta/cuesta 2001) as occurring in either primary psychotic or affective disorders.

So I am having trouble grasping the thesis you are advancing with your admittedly erudite recounting of psychiatric history.

Is the contention that catatonia, properly defined, is always and everywhere the result of a psychotic process?
 
So I am having trouble grasping the thesis you are advancing with your admittedly erudite recounting of psychiatric history.

Is the contention that catatonia, properly defined, is always and everywhere the result of a psychotic process?

No. The point is a lot of people think that catatonia is the result of depression that becomes so severe with such "stuporous" psychomotor ******ation that leads to (or is catatonia). That's why the diagnostic criteria and history/exam is so crucial, as shown by peralta/cuesta. The Kraepelinian conceptualization (in schizophrenia) is an "end stage" of volitional destruction resulting in a complete loss of the external/internal interface. I see this as a parallel to the one time primacy of passivity experiences in diagnosing schizophrenia.

Of course you can see catatonia in autism, limbic encphalitis, various medical conditions, etc, but the Abrams/Taylor classic study shows a predominance (62% in mania, 9% "endogenous depression") in affective illness vs scz (7%). However this was conducted using their own criteria (not Feighner, which was putative at that time), and one of my attendings who had collaborated before with them found that they tended to over diagnose mania.
 
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