Overview of Anticholinergic Medications

Transcript

Desiree Matthews: Welcome, everyone. Today, we're going to be discussing anticholinergic burden and practical strategies for deprescribing. My name is Desiree Matthews. I'm a board-certified psychiatric nurse practitioner, and today, we have two of my lovely colleagues, Dr Jonathan Meyer and Dr Leslie Citrome, with us here today.

Dr Jonathan Meyer: Hi, my name is Jonathan Meyer. I'm a voluntary clinical professor of psychiatry at the University of California in San Diego.

Dr Leslie Citrome: I'm Dr Citrome. I'm a clinical professor of psychiatry and behavioral sciences at New York Medical College in Valhalla, New York.

Desiree Matthews: Thank you. Today, we're going to be having a wonderful discussion about understanding anticholinergic medications and how they act both centrally and peripherally. We also want to discuss how that may lead to unintended drug side effects. We're also going to learn how to use available tools on how to calculate anticholinergic burden as well as discuss practical strategies today to help guide patients and care partners through that deprescribing process, including methods to avoid cholinergic rebound.

So, the first thing is, let's talk about just a broad overview for the audience about anticholinergic medications. First, can you give maybe a few examples of anticholinergic medications that are common in psychiatry?

Dr Meyer: In our clinical practice, we typically use medicines as psychiatric providers primarily for the mitigation of drug-induced movement disorders such as parkinsonism, and that's where the primary effect is—occasionally acute dystonia. Unfortunately, we sometimes use these medicines, which are anticholinergic, for other purposes, like the anticholinergic antihistamine diphenhydramine for sleep. We have other medicines that have anticholinergic properties, but we're typically not using them for that purpose; it's just an unintended feature of the molecule itself.

Desiree Matthews: Absolutely. Could you maybe describe to us a little bit, how they work? What neurotransmitter pathways are involved? And are there different receptors that acetylcholine signals through?

Dr Citrome: Well, actually, before we get into that, which is a very important aspect of what we need to discuss, I'd like to build upon what we've already said about its common use in psychiatry. There are also misuses, and I think we need to get that out of the way first. For example, the use in akathisia—it doesn't work in akathisia. Then, the prophylactic use of, let's say, benztropine for drug-induced parkinsonism that extends over a very prolonged period of time, like forever. Lots of our patients are on this, and they are centrally acting and peripherally acting. Now, we can get started on their mechanism.

Dr Meyer: The mechanism that we're using is blocking muscarinic and cholinergic receptors— we'll talk about this in a second—but there are two large families of coreceptors. One of these is nicotinic, which is involved in fast neurotransmission, such as at the musculoskeletal junction. We're talking about G-protein-coupled receptors and when we're using them appropriately, and I fully agree with Dr Citrome’s comments; a lot of the use out there is completely inappropriate. The intended use for drug-induced movement disorders has to do with mitigating the cholinergic-dopaminergic balance in the striatum. When I make somebody Parkinsonian, I've thrown that balance off; when I block the cholinergic signal, I can restore balance, and the person is no longer Parkinsonian. The same is true for acute dystonia as well. As was alluded to not, effective for akathisia. Another one, they do not work for tardive dyskinesia; they tend to make it worse.

Dr. Citrome: But you know, there's a long, illustrious history of using these agents for Parkinson's disease, and drug-induced Parkinsonism shares very similar problems in terms of dopaminergic signaling in the motor striatum. So, it does help with that. The problem is that it can be overused for too long, which can create some problems.

Desiree Matthews: What kind of side effects, potentially, could we see from using these anticholinergic medications, such as drug-induced Parkinsonism?

Dr Meyer: So, I’ll break them down into two sections, peripheral and central. I'll do the peripheral one and elect Dr Citrome to do the central one. Peripherally, a big part of the anticholinergic burden are the things that patients will complain about because we block certain signaling: dry mouth, constipation, blurred vision, and sometimes tachycardia. This is very common. If it becomes severe, urinary retention predominantly in males. And, you can also impair cholinergic-mediated sweating. This is why we look at package inserts for many molecules that are anticholinergic. They talk about the fact that you can have problems when you have more anticholinergics involved, and the person doesn't sweat well. But the central one, I think, is even more important. I'll let Dr Citrome describe that.

Dr Citrome: Yeah, unfortunately, exposure to centrally acting anticholinergic agents will impair cognition. It's actually used as a model for this when we're looking at cognitive abilities. This is a huge problem because let's think about where we use medicines like benztropine. We use them for people who already have impairments, to begin with, their cognition. So, to me, that is the major problem with anticholinergic load.

Desiree Matthews: Well, I think that's all we have time for now, but as always, It was wonderful to have this discussion with you guys today. Thank you, everyone, for joining us on this topic about anticholinergics with good colleagues of mine. If you want to learn more about this topic or other mental health topics, please visit Psych Congress Network to learn more.