Benzos vs benztropine for EPS in the elderly

[Stagg737]

So I got an outpatient consult recently for med recs on an 65ish year old lady with well-documented late-onset schizophrenia (onset around 52-53) who has been on Invega LAI for years and done very well with it. Patient and daughter are adamant about staying on it, as apparently previous periods without meds were disastrous. She's also been taking benztropine 1 mg BID for EPS (appears to be parkinsonism and akathisia) and clonazepam 1 mg daily for anxiety. When clonazepam was previously decreased minimally, daughter said EPS seemed to worsen (description does not sound like withdrawal), but lately patient has been complaining more of foggy thought process and some memory issues. Patient and mom think both are helpful for her EPS and are somewhat hesitant to decrease either one. I split the benzo dose to 0.5 mg BID for now with plan to decrease further, but trying to figure out which is the best to taper/decrease first. Problem is they were both started around the same time 2-3 years ago which is around when patient and family initially started having recognizing the cognitive issues.

Got me thinking about which of the two is actually a bigger risk for her in terms of cognition seeing as she's on a relatively low dose of clonazepam and a decent dose of benztropine. Patient and family want to address the cognitive concerns but don't want to touch the LAI. I'd like to know other's thoughts on the risk/benefit of benztropine vs clonazepam for her in terms of both the long-term and short-term cognitive effects.

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[WisNeuro]

I'd say there are 2 meds that I can see the biggest improvement in cognition when decreased or discontinued, oxybutynin, and benztropine.

 

[ObsequiousAplomb]

My opinion is that the benztropine is more likely contributing to cognition issues.

 

[Batman's Underwear]

agreed with benztropine as above. Later on what about other agents for parkinsonism like amantadine? Yes amantadine induced psychosis can happen but it is rare.

 

[psych_0]

The evidence for benzos and dementia is weak at best, with almost every study/meta-analysis etc reporting odd ratios (OR) well under 2. Statistically significant, sure (OR>1, I get it). Clinically significant, I would argue no. My vote would be to get rid of benztropine.

 

[WisNeuro]

The evidence for benzos and dementia is weak at best, with almost every study/meta-analysis etc reporting odd ratios (OR) well under 2. Statistically significant, sure (OR>1, I get it). Clinically significant, I would argue no. My vote would be to get rid of benztropine.

While I agree with the equivocal findings about dementia risk, people definitely perform as if they have dementia (depending on several factors) on testing and in day-today activities in benzos. That clears up with tapering or discontinuation. I still agree that the benztropine is most likely the biggest contributor in the above specific case, though.

 

[psych_0]

While I agree with the equivocal findings about dementia risk, people definitely perform as if they have dementia (depending on several factors) on testing and in day-today activities in benzos. That clears up with tapering or discontinuation. I still agree that the benztropine is most likely the biggest contributor in the above specific case, though.

Interesting. Which factors does it depend on?

 

[WisNeuro]

Interesting. Which factors does it depend on?

Usually things like dosage, how often its scheduled, when its scheduled, current liver function, among others. Though I only see a small percentage of people who taper down or discontinue in my clinic. Most of those are on maintenance benzos and have been for some time. Usually for mild to moderate anxiety.

 

[psych_0]

Usually things like dosage, how often its scheduled, when its scheduled, current liver function, among others. Though I only see a small percentage of people who taper down or discontinue in my clinic. Most of those are on maintenance benzos and have been for some time. Usually for mild to moderate anxiety.

Those are a lot of factors to say broadly that "people definitely perform as if they have dementia." Sounds more like "people definitely perform as if they have dementia [if they're on high doses with poor liver function and take 2mg right before our testing]" but idk.

 

[WisNeuro]

Those are a lot of factors to say broadly that "people definitely perform as if they have dementia." Sounds more like "people definitely perform as if they have dementia [if they're on high doses with poor liver function and take 2mg right before our testing]" but idk.

Generally try to get them to not take it the morning of the testing, still has an effect even with this, but that's about the best we can do to minimize the continued effects.

 

[annoyedpsychiatrist]

Have you considered propranolol for akathesia? Remeron has some evidence too.

I dont like klonopin in this scenario due to the half life, and i think a shorter acting benzo may be more ideal to reduce potential for side effects give her age, if you go with the benzo route.

Does she have the classic short shuffling gait/magnetic gait or is it more blunted express, unilateral tremor, stooped posture etc?

I think timeline of symptoms are really important too. Essential tremors in head/hands are common in elderly too and theres a lot of overlap in symptoms. Was the tremor there before the antipsychotic use? What was the timeline/progression of sx?

Hell is it possible she has parkinsons? You mentioned this was all late onset (which happens sometimes of course but usually less common) and you can have psychosis in parkinsons.

You may have thought of a lot of this already, but just my initial thoughts.

If I was going purely between klonopin vs cogentin I would prefer cogentin. I feel like theres more fall risk with klonopin. Low dose cogentin its a risk vs benefits sorta deal, but have used before in geri patients when needed and most seemed to tolerate it ok, but obviously the goal is to limit antichlonergic.

 

[Candidate2017]

Either med works for akathisia, anxiety, and EPS. I'd use only one med, at half dose, for a geri patient. Probably benzotropine. Keep in mind the long half life of Klonopin can cause it to build up in the elderly.

The real question, to me, is whether some side effects need to be treated. How severe is the EPS? Most patients don't mind mild to moderate EPS, while most patients do mind mild akathisia. So maybe only propranolol is needed. And of course, most patients who complain of anxiety don't have an anxiety disorder or one that rises to the level of needing a controlled sub.

The other overarching issue is many psychiatrists never discuss the natural history of psychiatric diseases to patients/families. This is a 65 year old who (and her family) has lived with schizophrenia, a brain disease that has damaged her brain, for decades. Cognition of an elderly schizophrenic cannot be expected to be the same as a non-schizophrenic of the same age, setting aside any iatrogenic anticholinergic or benzo issues. Even in the best of circumstances, the life expectancy of schizophrenics is 10-15 years lower. At 65, this patient and family need a discussion of what to expect and have expectations managed.

 

[Stagg737]

Thanks all, I'm leaning towards stopping the benzotropine first but just wanted to see what others' thoughts were.

The evidence for benzos and dementia is weak at best, with almost every study/meta-analysis etc reporting odd ratios (OR) well under 2. Statistically significant, sure (OR>1, I get it). Clinically significant, I would argue no. My vote would be to get rid of benztropine.

Yea, the data is pretty poor, and if I talk to patients about the dementia risk with benzos I mention that. I always have a higher level of concern for that when an elderly patient is already c/o cognitive issues though. Any way to minimize that risk is worth discussing IMO.

The other overarching issue is many psychiatrists never discuss the natural history of psychiatric diseases to patients/families. This is a 65 year old who (and her family) has lived with schizophrenia, a brain disease that has damaged her brain, for decades. Cognition of an elderly schizophrenic cannot be expected to be the same as a non-schizophrenic of the same age, setting aside any iatrogenic anticholinergic or benzo issues. Even in the best of circumstances, the life expectancy of schizophrenics is 10-15 years lower. At 65, this patient and family need a discussion of what to expect and have expectations managed.

That's the thing though, she hasn't had the bolded in this case. She was diagnosed with schizophrenia ~10 years ago, had a period of about one year on and off of being unstable (classic psychosis, would stabilize with antipsychotics and decompensate without them), and since then hasn't had any actual episodes of psychosis. This is per family who was present during the encounter who also said she hadn't had any symptoms remotely like those episodes other than some minimal transient paranoia.

She does have an affect somewhat reminiscent of true schizophrenic patients in that some of the more common microexpressions just aren't there or are noticeably blunted, but I do also wonder if she is truly schizophrenic or if there is something else going on.

 

[Stagg737]

Lots of good questions. Hopefully, the below can clarify a bit, but keep in mind this is in a collaborative care setting.

Have you considered propranolol for akathesia? Remeron has some evidence too.

Not yet, I don't want to make too many changes at once and they are very hesitant to make any changes at all since she's been stable so long. They actually asked about increasing the Invega, which I advised against right now.

I dont like klonopin in this scenario due to the half life, and i think a shorter acting benzo may be more ideal to reduce potential for side effects give her age, if you go with the benzo route.

I get that concern, but she was previously taking it once a day and I'm hoping that by splitting the dose she gets a more stable level as well as a slightly lower one as well as making a potential taper easier. I have thought about switching to lorazepam, but again don't want to make too make changes.

Does she have the classic short shuffling gait/magnetic gait or is it more blunted express, unilateral tremor, stooped posture etc?

I think timeline of symptoms are really important too. Essential tremors in head/hands are common in elderly too and theres a lot of overlap in symptoms. Was the tremor there before the antipsychotic use? What was the timeline/progression of sx?

Unfortunately, this is telehealth and I can't really get a good idea of her symptoms as they aren't obvious on the video. I was able to see her upper body and didn't notice anything. The EPS-like symptoms have been there the past few years and haven't had significant progression but are annoying. I also haven't ruled out a TD component. I can't do a formal AIMS, but I didn't see any facial, UE, or torso movements.

Hell is it possible she has parkinsons? You mentioned this was all late onset (which happens sometimes of course but usually less common) and you can have psychosis in parkinsons.

It's possible that she's developing it Parkinson's dz, but the initial episode sounds like pretty classic psychosis and nothing like Parkinson's psychosis. If it were in that spectrum, I'd be more worried about LBD which there doesn't seem to be any evidence of at this point.

 

[annoyedpsychiatrist]

Lots of good questions. Hopefully, the below can clarify a bit, but keep in mind this is in a collaborative care setting.


Not yet, I don't want to make too many changes at once and they are very hesitant to make any changes at all since she's been stable so long. They actually asked about increasing the Invega, which I advised against right now.


I get that concern, but she was previously taking it once a day and I'm hoping that by splitting the dose she gets a more stable level as well as a slightly lower one as well as making a potential taper easier. I have thought about switching to lorazepam, but again don't want to make too make changes.


Unfortunately, this is telehealth and I can't really get a good idea of her symptoms as they aren't obvious on the video. I was able to see her upper body and didn't notice anything. The EPS-like symptoms have been there the past few years and haven't had significant progression but are annoying. I also haven't ruled out a TD component. I can't do a formal AIMS, but I didn't see any facial, UE, or torso movements.



It's possible that she's developing it Parkinson's dz, but the initial episode sounds like pretty classic psychosis and nothing like Parkinson's psychosis. If it were in that spectrum, I'd be more worried about LBD which there doesn't seem to be any evidence of at this point.

i hate telehealth for patients like these because I feel like i dont get a clear picture and miss out on stuff. I dont mind tele for my ADHD/mild or moderate acuity people but i find tele is annoying for my psychosis patients. Though i understand some people have transportation issues. perhaps im old school

I think the biggest factor is what improves her quality of life. Likely low dose cogentin wont set her over the edge or even low dose benzos but i think monitoring for falls is always good

 

[Stagg737]

i hate telehealth for patients like these because I feel like i dont get a clear picture and miss out on stuff. I dont mind tele for my ADHD/mild or moderate acuity people but i find tele is annoying for my psychosis patients. Though i understand some people have transportation issues. perhaps im old school

I think the biggest factor is what improves her quality of life. Likely low dose cogentin wont set her over the edge or even low dose benzos but i think monitoring for falls is always good

Same with telehealth, but this clinic sees rural patients. And by rural I mean truly BFE where there’s one psych clinic within 2-3 hours. One of my patients last week was ~7 hours away in another time zone.

 

[annoyedpsychiatrist]

Same with telehealth, but this clinic sees rural patients. And by rural I mean truly BFE where there’s one psych clinic within 2-3 hours. One of my patients last week was ~7 hours away in another time zone.

is this community psych?

 

[hallowmann]

Same with telehealth, but this clinic sees rural patients. And by rural I mean truly BFE where there’s one psych clinic within 2-3 hours. One of my patients last week was ~7 hours away in another time zone.

Do they at least come into a clinic/CMHC for vitals with an MA/LPN/RN for the intake? If so, AIMS can certainly be done by staff, and is reasonably easy to teach if they don't know how to do it already. This is what is done for the telepsych patients I see in rural-middle of nowhere USA (many of whom also travel 2+ hrs to get to that clinic).

I agree, evaluating for EPS is not ideal with straight telepsych.

 

[WisNeuro]

Do they at least come into a clinic/CMHC for vitals with an MA/LPN/RN for the intake? If so, AIMS can certainly be done by staff, and is reasonably easy to teach if they don't know how to do it already. This is what is done for the telepsych patients I see in rural-middle of nowhere USA (many of whom also travel 2+ hrs to get to that clinic).

I agree, evaluating for EPS is not ideal with straight telepsych.

While not 100% ideal, I believe that there are studies looking at reliability of telehealth vs. in -person given a protocol that showed good equivalency. We looked into this during the pandemic when I was still in a hospital setting. Even back then there were some published protocols for it, I have to assume that there'd be even more done by this point with the expansion of telehealth.

 

[hallowmann]

While not 100% ideal, I believe that there are studies looking at reliability of telehealth vs. in -person given a protocol that showed good equivalency. We looked into this during the pandemic when I was still in a hospital setting. Even back then there were some published protocols for it, I have to assume that there'd be even more done by this point with the expansion of telehealth.

I buy equivalency in certain metrics, for example remission rates, reduction in hospitalizations, etc., because much of what we do doesn't necessarily require a physical exam. The area I think that is much harder to quantify are examples like this where its very difficult to evaluate these types of adverse effects without an exam, especially depending on the severity of illness of the population being evaluated (most of whom often have SMI).

Ways around this are typically by having a clinic the patient is physically coming to with staff trained to evaluate or alternatively wearables and other diagnostic devices that patients can be issued (usually a bigger issue in other specialties).

 

[WisNeuro]

I buy equivalency in certain metrics, for example remission rates, reduction in hospitalizations, etc., because much of what we do doesn't necessarily require a physical exam. The area I think that is much harder to quantify are examples like this where its very difficult to evaluate these types of adverse effects without an exam, especially depending on the severity of illness of the population being evaluated (most of whom often have SMI).

Ways around this are typically by having a clinic the patient is physically coming to with staff trained to evaluate or alternatively wearables and other diagnostic devices that patients can be issued (usually a bigger issue in other specialties).

I was referring to scores on the AIMS scale, specifically, when referencing the reliability between the two methods. If I have time, I'll see if I can track down any of what we looked up back then, if I still have those files somewhere.

 

[hallowmann]

I was referring to scores on the AIMS scale, specifically, when referencing the reliability between the two methods. If I have time, I'll see if I can track down any of what we looked up back then, if I still have those files somewhere.

You mean obtaining scores only via video? I don't know, sometimes I can barely get patients to show me their whole face when I'm doing video visits at their home, so maybe this is more about the population I treat... Would be interested in the article if you can find it

 

[WisNeuro]

You mean obtaining scores only via video? I don't know, sometimes I can barely get patients to show me their whole face when I'm doing video visits at their home, so maybe this is more about the population I treat... Would be interested in the article if you can find it

We never had much of a problem getting patients to do some things like gait demo and extremity observations in the late 2020/early 2021 when we were all virtual for neuro evals. But these were generally dementia, traditional movement disorders stuff.

 

[Stagg737]

is this community psych?

Nope, large academic center.

Do they at least come into a clinic/CMHC for vitals with an MA/LPN/RN for the intake? If so, AIMS can certainly be done by staff, and is reasonably easy to teach if they don't know how to do it already. This is what is done for the telepsych patients I see in rural-middle of nowhere USA (many of whom also travel 2+ hrs to get to that clinic).

I agree, evaluating for EPS is not ideal with straight telepsych.

Not always. Many evals are from their home or other locations, so I'm often not even getting reliable vitals which limits my options for some people.

 

[annoyedpsychiatrist]

You mean obtaining scores only via video? I don't know, sometimes I can barely get patients to show me their whole face when I'm doing video visits at their home, so maybe this is more about the population I treat... Would be interested in the article if you can find it

half the time in the really sick patients, they struggle to figure out how to use the webcam and I end up with an image the freezes every two seconds and audio that looks like it was dubbed, lol. Or sometimes it will be people in the car driving. I hate when that happens ugh lol. Sometimes even a brief observation of gait as they walk into my office gives me some good info to go off of. Its the small things you miss in tele with patients like these, but I feel like each part adds relevant info to the overall picture.