Not feeling comfortable prescribing Benzo's?

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Avoidance isn't a necessary component of anxiety. Anxiety is not by itself pathological.

It's the pathologic avoidance that we're circumventing by making someone more comfortable for the MRI.

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It's the pathologic avoidance that we're circumventing by making someone more comfortable for the MRI.

Again, I actually think we generally agree but I don't even think there's a need to determine whether or not the avoidance is pathological before we do these interventions (this was my major disagreement with one of the psychologists in this thread). This is why I have been making so many comparisons to anesthesia.

If somebody told the orthopedist they weren't going to let them reduce their fracture without some sort of analgesia/local anesthesia, I don't think this is pathological. This type of procedure, based on a physiological response, is going to cause a degree of pain that is going to be intolerable to a fair number of otherwise normal people. There are a lot of variables so I don't really know for sure whether the avoidance is pathological in an individual patient, but it likely isn't. Either way, I don't really care. Making other necessary care viable is enough of an indication for medication. I don't really think that it's necessary to determine whether the barrier the medication is ameliorating is part of a pathology (at least not immediately).
 
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It's generally accepted that long-term benzo use can contribute to, if not trigger, cognitive decline, particularly with regard to visual-spatial and attentional deficits. I have run across some articles challenging this claim, but that's the general consensus.

Benzodiazepine use and cognitive decline in elderly with normal cognition

Benzodiazepine use and risk of incident dementia or cognitive decline: prospective population based study

So I got around to checking out these references, and I'm not really impressed with the notion that benzo use has a causal relationship with cognitive decline, particularly irreversible.

The first paper, "All participants who reported taking BZDs had poorer cognitive performance at all visits than nonusers. However, cognitive decline was statistically similar among all participants. We found no evidence of an association between BZD use and cognitive decline. The poor cognitive performance in BZD users may be due to prodromal symptoms caused by preclinical dementia processes."

The next one, "The risk of dementia is slightly higher in people with minimal exposure to benzodiazepines but not with the highest level of exposure. These results do not support a causal association between benzodiazepine use and dementia."

Granted, I'm not suggesting that we start feeding them to Gramma every day with her morning oatmeal. I get that they're like, super bad for the elderly for so many reasons.

But if you're going to suggest that a psychoactive drug has a causal, or hell, even an observable association with cognitive decline, particularly irreversible, I think that deserves a question. I'm the last person on this board to demand a link to a study. I took what you said at face value beyond just wanting some more clarification.

I know you said there was some mixed results out there, but I didn't expect the two sources you cited supporting your point to, basically not support it at all. I'm not trying to be a dick. I just am surprised at how this turned out.

ETA: I didn't just check out the conclusions. I looked at the study designs as well.
 
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I don't see taking APAP for a headache now and again as pathological. Hell, that goes for taking an opioid for the occasional this or that.

It's OK to use modern medicine, and even controlled substances, and even ones with abuse potential, to be more comfortable sometimes within reason. The number one ingredient in liquid Nyquil is alcohol. It's OK to have a shot or two of booze to help with the symptoms of your occasional head cold.

For some of you, it sounds like there is never a reason. That is just not how I would practice. I don't see everything in terms of pathology, and I think it's OK to sometimes just make people more comfortable without getting into major hand wringing about it.

Granted, the patients going to a psychiatrist and wanting a benzo present a different challenge.
 
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I know you said there was some mixed results out there, but I didn't expect the two sources you cited supporting your point to, basically not support it at all. I'm not trying to be a dick. I just am surprised at how this turned out

I think you misunderstood the point of those links. I said they were links to studies challenging the claim that benzo use leads to cognitive decline, though reading back on my post, it is confusing. Sorry if that wasn't clear.
 
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Benzos also can be quite helpful for folks with psychotic disorders or bipolar 1. Anecdotally if you have someone on good antipsychotic or mood stabilizer then they are starting to decompensate a little, adding some Klonopin at night can sometimes pull things back together and may save an inpatient admission.
... or their life
 
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So I got around to checking out these references, and I'm not really impressed with the notion that benzo use has a causal relationship with cognitive decline, particularly irreversible.

The first paper, "All participants who reported taking BZDs had poorer cognitive performance at all visits than nonusers. However, cognitive decline was statistically similar among all participants. We found no evidence of an association between BZD use and cognitive decline. The poor cognitive performance in BZD users may be due to prodromal symptoms caused by preclinical dementia processes."

The next one, "The risk of dementia is slightly higher in people with minimal exposure to benzodiazepines but not with the highest level of exposure. These results do not support a causal association between benzodiazepine use and dementia."

Granted, I'm not suggesting that we start feeding them to Gramma every day with her morning oatmeal. I get that they're like, super bad for the elderly for so many reasons.

But if you're going to suggest that a psychoactive drug has a causal, or hell, even an observable association with cognitive decline, particularly irreversible, I think that deserves a question. I'm the last person on this board to demand a link to a study. I took what you said at face value beyond just wanting some more clarification.

I know you said there was some mixed results out there, but I didn't expect the two sources you cited supporting your point to, basically not support it at all. I'm not trying to be a dick. I just am surprised at how this turned out.

ETA: I didn't just check out the conclusions. I looked at the study designs as well.

I'd suggest checking out some more research, those two articles cited contained horrible methodology. I actually teach medical residents about the hazards of using things like screeners and inappropriate modeling in degenerative conditions research. It's why people think things like dozepezil are useful. One of the links I posted has a meta-analysis that contains the references to the studies included if you are so inclined.
 
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It never seems like dozepezil is doing anything until you stop it. I agree it doesn't change the slope of the memory loss, but it does back you up half a year. I don't think anyone claims it does anything more and I would take it if I were dementing.
 
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It never seems like dozepezil is doing anything until you stop it. I agree it doesn't change the slope of the memory loss, but it does back you up half a year. I don't think anyone claims it does anything more and I would take it if I were dementing.

If you look at the actual data, it does not do this. The only thing there is real evidence of, is reducing some problematic behaviors temporarily, but there are probably better ways to do this considering the high rates of GI problems with donepezil.
 
It never seems like dozepezil is doing anything until you stop it.

In regards to Donepezil, what I suspect is going on is the patient does get somewhat better, that becomes the new normal and they forget it caused improvement. This is often times what happens with a lot of psych meds like antidepressants but with Donepezil we got a cognitively-impaired person whose memory will only worsen and will likely forget the benefits it caused. E.g. the patient who takes an antidepressant, is better for it, takes it for a few months then after feeling good for that time decide to stop the med without consulting the psychiatrist.

In patients with alcohol-induced dementia and other forms that don't have such as steady and quick course of decline I've noticed more patients don't forget it caused a benefit and are happier with continued use of it.
 
In regards to Donepezil, what I suspect is going on is the patient does get somewhat better, that becomes the new normal and they forget it caused improvement. This is often times what happens with a lot of psych meds like antidepressants but with Donepezil we got a cognitively-impaired person whose memory will only worsen and will likely forget the benefits it caused. E.g. the patient who takes an antidepressant, is better for it, takes it for a few months then after feeling good for that time decide to stop the med without consulting the psychiatrist.

In patients with alcohol-induced dementia and other forms that don't have such as steady and quick course of decline I've noticed more patients don't forget it caused a benefit and are happier with continued use of it.

Seriously, even when you take into account the inappropriate use of LOCF, which artificially boosts the purported effect size, you are still at about a maximum of 1/3 of the difference needed to determine clinically significant change on cognitive measures for large scale studies of donepezil. A 1.2 difference in MMSE, or 2 point difference in the ADAS-Cog are not meaningful in any clinical sense. Additionally, there has been no stout finding of identifying any group that could possibly be a "responder" to treatment (e.g., APOE status, familial history, age of onset, etc). What you are actually seeing is the brief period of a placebo, because something is being done, with a possible temporary benefit of decreased problematic behaviors, which quickly washes out, leaving the patient with no benefit and more diarrhea.
 
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Admittedly, it has been a long time since I have worked inpatient Geri, but those that do tell me that they stop all meds except Donepezil and watch people get better. When you ask them why Donepezil, they say because patients crash and burn when you stop it. Not very data driven or scientific, but I have heard this more than once.

As far as clinical significance, we have lots of drugs boasting superiority over other drugs quoting statistical significance. When you treat something as hopeless as progressive dementia, your standards are embarrassingly low.

Like everything, it works well for a few and does nothing for a lot. The trick is to give it a shot and remember that it is a trial and if the risks outweigh the benefits, stop it. Personally, I would give it a shot if I were dementing. Even if it kept me out of the diaper phase for only an extra two months, I would want it.
 
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Admittedly, it has been a long time since I have worked inpatient Geri, but those that do tell me that they stop all meds except Donepezil and watch people get better. When you ask them why Donepezil, they say because patients crash and burn when you stop it. Not very data driven or scientific, but I have heard this more than once.

As far as clinical significance, we have lots of drugs boasting superiority over other drugs quoting statistical significance. When you treat something as hopeless as progressive dementia, your standards are embarrassingly low.

Like everything, it works well for a few and does nothing for a lot. The trick is to give it a shot and remember that it is a trial and if the risks outweigh the benefits, stop it. Personally, I would give it a shot if I were dementing. Even if it kept me out of the diaper phase for only an extra two months, I would want it.

The only long-term studies that exist, as most just use models that project long-term, actually show no change in time to disability and/or NH placement. If anything, the treatment group had higher medical costs through the course of the study period (correcting for med cost of donepezil). Also, there's an easy way to counter the issue of a discontinuation effect of a medication that does not act in its intended purpose. Not prescribe it in the first place. Looking at the data, the risks/adverse effects of this drug vastly outweigh any benefits. It's a prime example of the power of misleading marketing, shady research practices, and prescribers not knowing the data behind what they are giving to patients.
 
The only long-term studies that exist, as most just use models that project long-term, actually show no change in time to disability and/or NH placement. If anything, the treatment group had higher medical costs through the course of the study period (correcting for med cost of donepezil). Also, there's an easy way to counter the issue of a discontinuation effect of a medication that does not act in its intended purpose. Not prescribe it in the first place. Looking at the data, the risks/adverse effects of this drug vastly outweigh any benefits. It's a prime example of the power of misleading marketing, shady research practices, and prescribers not knowing the data behind what they are giving to patients.
Or prescribers who are sick of arguing with patients over a now cheap and fairly benign drug.
 
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