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EngageTD: Workshop-Based Training in Tardive Dyskinesia Evaluation and Personalized Care

The Unique Role of APPs in Detection and Management of TD

Introduction:

Jeremy Schreiber:

Good evening, everyone. Thank you so much for joining us. This is EngageTD: Workshop-Based Training in Tardive Dyskinesia Evaluation and Personalized Care. Now, this is brought to you by Decera Clinical Education. It is a 90-minute webinar, and it is supported by an educational grant from Teva. I would like to thank you very much for attending this evening.

Faculty

I am Jeremy Schreiber. I am a psychiatric-mental health nurse practitioner, adjunct faculty at West Liberty University, and the founder, CEO, and a practicing psychiatric-mental health nurse practitioner at Enlighten Health Care, LLC in Wheeling, West Virginia. One of our other esteemed faculty members with us tonight is Eric Carlon. He is a psychiatric-mental health nurse practitioner who practices at the Home Physicians Group, and he serves as clinical faculty for a few different universities and is in Florida. He is very fortunate to be in Florida. We also have Jayson Gesulga. He is a physician assistant practicing at Holistic Psychiatry in West Des Moines, Iowa, as a breakout moderator.

Disclosures

You can see all of our disclosures here.

Learning Objectives

The learning objectives for this presentation and webinar tonight are to help us become very proficient at assessing our patients for tardive dyskinesia and knowing how to treat them. Some of that relates to being proactive with our risk stratification and monitoring strategies to identify these patients, and then counseling our patients about the utilization of antipsychotic medications, and understanding who is at a heightened risk for tardive dyskinesia.

On top of that, we are going to talk about validated screening tools, and not only talk about them, we are going to apply them to see how these work in clinical practice when we are examining patients in front of us. Knowing how to perform the Abnormal Involuntary Movement Scale exam is fundamentally important. We will also talk about how to integrate this into the routine clinical workflow, how to document this, and how to follow up in diverse care settings.

We will talk about the efficacy, safety, and tolerability profile of the FDA-approved VMAT2 inhibitors, using the products that are FDA-approved, and how we can individualize these treatments in terms of the pharmacological management of tardive dyskinesia in older adults and special populations as well.

Workshop Agenda

Welcome to the introduction and setting the stage. We are going to talk about how advanced practice providers are situated in a unique position to monitor and benefit our patients because we have excellent relationships with our patients and are frontline providers with them. We will talk about age-related vulnerability and early recognition. We will go into some breakouts. When we go into these breakouts, you will have the ability to ask questions via the chat. You also have the ability to raise your hand, and we may be able to call on you there, which is nice.

We will talk about mastering the AIMS exam and how we integrate this into our workflow. There is a practice section here in terms of scoring an AIMS exam. If you see on the bottom right of your screen, it says download the PDF of the AIMS worksheet, which is under the resources tab. When you go to resources, inside of that resources section, there is a tab that says documents. That is where you can find the downloadable PDF for the AIMS worksheet. We are going to review the AIMS scoring, monitoring, how the routine workflow goes, and why we are evaluating patients when we see them.

We will practice scripting treatment recommendations and discuss the evidence base supporting these VMAT2 inhibitors. In other words, show me the efficacy and show me the safety data. Why should I be considering these? Then we will do key takeaways, followed by a question-and-answer session. At the very end, I will talk to you all about how to claim your continuing education credit for this 90-minute webinar.

The Unique Role of APPs in Detection and Management of TD

We are going to talk about the unique role that advanced practice providers play in both detecting and managing tardive dyskinesia. The reality is that there is a plethora of advanced practice providers, and we tend to be frontline providers, especially in psychiatric settings, primary care settings, and other environments. Because of that, our role in treating patients is centralized. We are looking at with our patients, having these very good patient relationships, and because of that, because we have these consistent relationships, we are integral to the process of both recognizing and managing it.

We are also very frequently managing these psychotropic regimens. On top of managing it in our own patients, we are often managing psychotropic regimens that have been initiated by other healthcare providers. Because of this, when other healthcare providers initiate antipsychotic medications and we are managing the patients, in other words, we may not be managing that particular antipsychotic medication, we still need to be looking at the symptoms and the adverse event profile in monitoring our patients because they may develop tardive dyskinesia.

We see our patients; we spend time with our patients; we look them up and down. The American Psychiatric Association recommends that for patients who are treated with antipsychotic medications, that we are at least doing a clinical once over every visit. One of the challenges with tardive dyskinesia is that the movements can be subtle, but oftentimes with tardive dyskinesia the symptoms evolve and can become worse. We also need to understand that our patients might not be aware of the symptoms, or patients may want to rationalize where their symptoms are coming from: something is wrong with my tooth, or dry lips, these kind of things.

If we can recognize and detect tardive dyskinesia earlier, then we can treat it and have meaningful improvement that hopefully helps enhance the quality of life for our patients that are suffering from this condition.

It says here it is frequently unrecognized, and statistics show that while 800,000 people or more have tardive dyskinesia, less than a quarter of these patients are diagnosed. It is really quite staggering. Even when patients are diagnosed, the number who are treated; I believe it is of the patients that are diagnosed, less than one in eight. I think that we have the ability to help our patients, and I appreciate you all being here with us tonight.

Age-Related Vulnerability and Early Recognition

Eric Carlon: Thanks, Jeremy. My name is Eric Carlon. I am a psychiatric nurse practitioner in Central Florida. I work primarily in long-term care settings, such as skilled nursing facilities and assisted living facilities. I see a lot of tardive dyskinesia within the older population and some of the effects it can have on them.

What Is Tardive Dyskinesia?

What is tardive dyskinesia? Tardive dyskinesia involves involuntary movements of specific parts of the body that occur after long-term treatment with dopamine receptor-blocking agents. A lot of times, you can see it in the face or the lips, pursed lips or eye blinking. It can also occur in the upper and lower extremities, and can even involve the diaphragm, affecting breathing to an extent. This is differentiated from withdrawal-emergent dyskinesia. The symptoms of tardive dyskinesia can wax and wane; as Jeremy was saying earlier, it goes up and down. Sometimes it is worse than others. It can also be temporarily masked if you increase the dose of a dopamine receptor-blocking agent.

Pathophysiology of TD

The pathophysiology of tardive dyskinesia, essentially the chronic blockade of dopamine receptors leads to an upregulation of dopamine receptors. These newly created receptors are hypersensitive. The endogenous dopamine that the patient already has will hook onto these new receptors and then cause the involuntary movements. Second-generation antipsychotics are less likely to cause tardive dyskinesia compared to first-generation agents, but they still can. There is also a genetic vulnerability that might factor into the development of tardive dyskinesia.

Diagnostic Criteria

The diagnostic criteria for tardive dyskinesia, DSM-5-TR defined tardive dyskinesia as a medication-induced movement disorder that persists despite the discontinuation or change of the medications. This is going to be a history of at least three months of taking a dopamine receptor-blocking agent, or in the older population aged greater than 60 years, a duration of just one month. These symptoms must then persist for greater than one month.

Differential Diagnosis of TD vs Other Drug-Induced Movement Disorders

I think this is a neat slide. It breaks down the differential drug-induced movement disorders that we will encounter. So you see the top one, the dystonia, that is going to be right after starting the medication. So within three days, that is a sustained contraction, very rigid. Several days to a week is that akathisia, that internal restlessness and the cannot sit still type feelings. Weeks to months is more of the drug-induced Parkinsonism. So, general slow movement, the bradykinesia in a tremor. And then tardive dyskinesia, that we see months to even years, and that is the more involuntary choreiform type movements.

Risk Factors for TD

Looking at risk factors, the modifiable risk factors, obviously higher cumulative doses of antipsychotics, both first-generation and second-generation. Co-treatment with anticholinergic agents. History of acute drug-induced movement disorders of patients that have taken these medications in the past and developed Parkinsonism or akathisia. Diabetes, smoking, and alcohol and substance use disorders. The nonmodifiable risk factors we are looking at: age greater than 50, postmenopausal status. So the longer duration of illness, these people have been taking these medications for a longer time. Also mood disorders, cognitive symptoms and mood disorders, as well as intellectual disability and brain damage and dementia.

Is the Older Population at Risk?

So looking at the older population, tardive dyskinesia is five to six times more prevalent in older patients. Why is that? Probably because these patients have longer exposure to medications. Patients in skilled nursing facilities are prescribed antipsychotic medications more often than older patients in the general population. You also see extrapyramidal signs earlier in the treatment. And then there is just an inherent age-related decrease in dopaminergic neurons in the older population. And then the other, lower doses of second-generation antipsychotics can trigger tardive dyskinesia.

Multifaceted Burden of TD on Patient Quality of Life

So we see the multifaceted burden of tardive dyskinesia on a patient's quality of life. So going from social patients, and in my setting, these patients do not want to leave their rooms. They do not want to take part in the activities. They just stay in their rooms all day, every day. They have the staff bring the meals to them because they do not want to go to the dining area. A lot of times they start to feel sad, down. They are anxious about the movements. Patients in the outpatient in the community setting, they struggle to get meaningful employment and maintain work. They will have issues with transportation, things like that. And then physical, what I see is the biggest thing is that when they start to have the movements in the hands, they have trouble eating. They cannot hold the utensils; they cannot hold cups. So a lot of times it gets to be where the staff say, hey, so-and-so is not eating all of their meal. They barely even picked up their breakfast or their lunch, or whatever it is. And then you have to investigate further and realize it is not really an appetite issue. It is more of they cannot physically put the food in their mouth.

An Additional Consequence of TD: Negative Impact on Medication Adherence

And then in addition to that, you can see your patients with tardive dyskinesia, almost half reported that they skipped a dose of their antipsychotic or even took less than what the doctor was giving them. Almost 40% stopped taking the antipsychotic medication altogether. Over a third stopped going to the doctor that was treating the underlying condition. And then one in five actually advised another patient to stop taking their antipsychotic medication.

Patient Case: Charles

So now we are going to look at Charles. Charles is a patient that you inherited from a colleague in your practice who is retiring. He is a 78-year-old man with schizoaffective disorder. He lives with his son and his daughter-in-law. They are not present at the visit today, but they are listed in the HIPAA release file in the chart. The narrative notes indicate he was diagnosed in his 30s, but dated records go back only to 2017. So he is currently on a paliperidone long-acting injectable, 156 milligrams. You see him; he is being seen once a month, so it allows for regular monitoring. He was initiated on the paliperidone LAI in 2017, and eventually titrated up to the current dose in 2018.

So in your initial interview, he seems to be doing well with no notable symptoms. He is well-groomed, clean. He smells like cigarettes, so you might think that he is a cigarette smoker. No items of concern on the routine PHQ-9 or BPRS. And he tells you he has been doing well since moving into this family about 20 years ago, but he has a history of unstable living situations and some hospitalizations over his life.

Jayson Gesulga: Hello, colleagues. I am a psychiatric physician assistant out of Des Moines, Iowa. I spent 8 years in community mental health, and the last 2 years I have been in private practice with Holistic Psychiatry. This part of the presentation is going to be our discussion. I encourage everyone to participate. This is how we learn. This is the essence of medicine.

Known TD Risk Factors: Charles

We will go back to our sample patient, Charles. The question was, are there any additional risk factors that we are worried about? Are there any known risk factors that really pop out at you guys? Feel free to unmute your microphone and tell me, or type it in the chat. You can also raise your hands.

Our colleague Eric Carlon went over some of those additional risk factors because we know that everyone taking an antipsychotic or dopamine receptor-blocking agent is at risk of developing this movement disorder we call tardive dyskinesia. But who is at additional risk? Perfect. I am seeing Sunshine over here saying medicated for about 48 years. Absolutely. The duration your basal ganglia is exposed to those medications is an additional risk factor.

I see there is a question: What other medications does he take? Okay. His age. Yes, his age. Absolutely. Thank you, Sharon. Thank you, Nisi, for those points.

This patient has several tardive dyskinesia risk factors. Age greater than 50 years is a nonmodifiable risk factor.

A second-generation antipsychotic carries a lower risk, but what about previous first-generation antipsychotics? He was diagnosed in the 1980s, so he has a history of long-term exposure.

What else would you ask to help determine his tardive dyskinesia risk? We need to look at modifiable risk factors like a history of acute drug-induced movement disorders, including akathisia, dystonia, or drug-induced Parkinsonism, which we often call extrapyramidal symptoms.

As our brain ages, we lose what we call a neuronal reserve. These neuronal reserves function like a buffer that helps manage chorea movements in the background. Charles is a current smoker, which definitely does not help things. He also has a history of multiple hospitalizations. These represent potential unknowns. I love those observations. You guys are doing great.

What about other contributing medications? We need to screen for anticholinergics like benztropine or trihexyphenidyl. Is there any history of alcohol or substance abuse, intellectual disability, or brain damage? These are all critical potential risk factors.

As we age, we lose some of that buffering capacity. When our brains are exposed to these dopamine receptor-blocking agents at the base level of the basal ganglia, a neurochemical reprogramming occurs – a maladaptive learning, if you will. Chorea is the background noise that is happening. When we have a neuronal reserve in a younger brain, you might not see that chorea coming out as much. That is why we use activation maneuvers during an Abnormal Involuntary Movement Scale exam to distract those buffering neurons, and the movements get worse for us. As we age, we lose that neuronal reserve, and that is an additional risk factor there.

Could we advance the slide, please? You guys are rock stars; you are getting them all.

Known TD Risk Factors: Charles

There you go. We can just click through those builds. Those are the exact items everyone mentioned.

Diagnosis of a mood disorder. I was a little quick there, but that item on the top – a diagnosis of a mood disorder over a psychotic disorder – is an interesting additional risk factor. Why is that? Anyone have any ideas? Please type them in the chat.

There are several pharmacological thoughts regarding that. When someone has a mood disorder, they may be exposed to what I call non-mood-stabilizing antidepressants, such as sertraline or fluoxetine. Those agents all have their specific nuances. We pride ourselves as psychopharmacologists who know all the properties of these SSRIs and SNRIs. They have different doses and receptor profiles, but all in all, they are essentially dunking your brain in a bucket of serotonin.

When that happens, it places the basal ganglia in a functional hypodopaminergic state. You have to follow all the different neurological pathways, but excess serotonin effectively primes the brain. When you later add a dopamine receptor-blocking agent like an antipsychotic, the brain is already primed and is much more apt to develop a hyperkinetic movement disorder like tardive dyskinesia. That is the current pathophysiological thought.

You guys also mentioned these potential key risk factors as well, like what other medications has he been on? His additional medical history. He is currently treated with a second-generation antipsychotic – the monthly paliperidone palmitate long-acting injectable – but his clinical history, this goes all the way back for many decades. Has he perhaps been exposed to first-generation antipsychotics in his past? We know that the prevalence rates for tardive dyskinesia with first-generation antipsychotics are up to 30%. That 30% prevalence rate compares to second-generation antipsychotics, which carry a lower baseline rate of about 7.4%. However, if a patient has past exposure to first-generation antipsychotics, that second-generation risk profile significantly increases to about 20.4%. Just that exposure to that could be a potential tardive dyskinesia risk factor as well.

Potential TD Risk Factors: Charles

He displays no current notable symptoms, but what about a history of negative or cognitive symptoms? As we saw in that additional risk factor slide, an additional risk factor could be any sort of what I like to think of different brain, so any sort of dementias or traumatic brain injuries, autism spectrum disorder, or intellectual disabilities. Those are additional risk factors for developing tardive dyskinesia.

And then also, any other contributing medications, for instance, anticholinergics. We know these anticholinergics do exist. I am talking about agents like benztropine or things like trihexyphenidyl, but also the over-the-counter anticholinergics you can find at your local pharmacy or grocery store, such as diphenhydramine and doxylamine, all these other anticholinergics. I challenge you to look at the over-the-counter drug section next time you are in a pharmacy and notice how many anticholinergics you can buy over the counter. We want to see if those are acting as contributing factors.

Cross-sectional studies show that benztropine is actually the number one risk factor for developing tardive dyskinesia. These anticholinergic medications were originally designed to increase movement. If we are managing a hypodopaminergic movement disorder like drug-induced Parkinsonism – where a patient presents with a blunted affect, a focal tremor, a little drooling, slumped shoulders, and rigidity on cogwheeling – then, yes, you can get some clinical benefit. That is an on-label indication for benztropine.

However, on that exact package insert, it explicitly states do not use it in tardive dyskinesia because it can make the symptoms worse or fail to help altogether. Tardive dyskinesia is a hyperkinetic movement disorder. Logically, we should not use a medication designed to increase movement in a system that is already experiencing a hyperkinetic movement disorder. That is the logic there.

We also screen for alcohol or substance abuse, intellectual disability, and any history of acute drug-induced movement disorders. Having a documented history of drug-induced Parkinsonism, akathisia, or dystonias significantly heightens your long-term risk of developing persistent tardive dyskinesia.

Risk Level Determines Screening Recommendations

Eric Carlon: So the risk level is going to obviously determine the screening recommendations. And you can see the risk factors there on the left. Patients older than 50 years old, potentially 3-5 times higher risk. History of previous drug-induced movement disorders. The dose, duration, and potency of their dopamine receptor-blocking agent that they are taking. Any history of substance use disorders, mood disorders. So it is recommended that patients that are high-risk and taking a first-generation antipsychotic, you are going to perform an AIMS exam on them every 3 months. Any patient taking a first-generation antipsychotic or high-risk and taking a second-generation antipsychotic, every 6 months. And then any patient taking a second-generation antipsychotic is every 12 months. And then it is also recommended that you could do the semi-structured exams, like Jeremy was mentioning earlier, in between your formal AIMS assessments. Anytime that you get a chance to be in front of your patient, you could be doing a quick little exam to take a peek at any abnormal movements.

AIMS Mastery and Workflow Integration

Jeremy Schreiber: All right, so now what we are going to talk about is the AIMS mastery and the workflow integration here. So what I am going to do is I am going to basically walk through and demonstrate how I typically perform an AIMS examination by assessing Eric. So that is what is going to happen here.

AIMS Examination Procedure

Let us see here very briefly. All right, so what you see here is the AIMS examination procedure. Again, this would be one of those things that you can find that worksheet in the resources documents place to pull up the AIMS worksheet. I would highly encourage you to do that.

Oftentimes, I am in clinical practice in person. I also do some remote work. Those of you that do remote work, I will talk about a little bit of strategies and things that I do when I am assessing patients via telehealth. But patients are much more likely to hide their movements from us. One of the things we want to do is we want to observe our patient at rest when they do not know they are being watched. Because if they do not know they are being watched, they are more likely to exhibit the symptoms. And by the way, two points that I want to make about that. If people are more likely to make movements when they are not being watched or when you are performing an AIMS exam, their movements become more paramount. This should already alert you as a provider that the symptoms are bothersome to the patients because they are spending mental effort to hide that for us.

So what I do, I go get my patients in the waiting room. I walk up, and let us say Eric is my patient. I am going to call Eric back. I open the door. I am checking him out for a minute. And I am like, Eric, come on back with me, or I will look at him through the reception window before I go grab him. I will bring him back to the office. And as he is coming back to the office, I am going to watch him walk. I want to see as he is walking, if he is making finger movements or mouth movements. Sometimes patients, when they are walking, they are concentrating on walking. So now they are not concentrating on hiding these movements from us. So they may reveal movements that they would not otherwise reveal.

What we want to do is we want to ask the patient, "Hey, Eric, do you have anything in your mouth? Gum, candy?"

Eric Carlon: No.

Jeremy Schreiber: No? Okay. If he did, we would ask him to remove that because if patients have gum or candy, they can make the mouth movements. It looks like they may have tardive dyskinesia but they probably do not if it is just gum or candy. Eric, do you wear dentures?

Eric Carlon: No.

Jeremy Schreiber: Okay, perfect. So you want to ask about the condition of the teeth. You want to ask about if patients are wearing dentures. And if they do have dentures, we should ask about if the dentures bother them. Because if someone has ill-fitting dentures, they tend to mess with them and manipulate them both with their jaw movements and with their tongue. The same thing happens when people get chips in their teeth. They will play with those with their tongue. They will move things around. It can look like tardive dyskinesia. So we are going to watch that.

And then what we do is we ask our patients, "Hey, have you noticed any movements in your mouth, your face, your hands, your feet, torso?"

Eric Carlon: No.

Jeremy Schreiber: Okay. If our patient says yes, ask them to describe them. See if they currently bother the patient, so to speak. And then what you want to do is you want to have your patient sit in a chair. So Eric, if I could have you move back just a little bit for me in the frame if that is possible. See if Eric can get back here. All right. Now, I do not know if you all can see Eric's hands. I assume that you can. The screen is a little bit bigger. But Eric, what I want you to do is I want you to sit in a chair, and I want you to put your feet flat on the floor for me.

Eric Carlon: Okay.

Jeremy Schreiber: Thank you very much. And while he is doing this, I am just giving him the up and down, the once over, seeing if he is making any abnormal movements.

And then what I do is I say, Eric, I want you to rest your hands on your knees with your hands dangling. So what that would look like is hands on the knees, but out so the fingers can dangle freely. Because if somebody has their hand on their knee or the arm of the chair, you will not be able to see them move. But if they are dangling, you can. So you want to watch for that. So if you could have your hands dangle, that would be great. Thank you. And then what I do is I mimic. So you ask the patient, "Hey, can you put your right arm out?" And so I usually hold out my left arm to be a mirror image. And I want you to tap your fingers to your thumb back and forth like this as quickly as you can.

While he is doing that, I am going to be looking at his face for movements. Now, for this particular portion, Eric, let me have you swing back up a little closer to the camera. So we are going to be looking as he is tapping his fingers for feet movements, trunk movements. Go ahead, put those hands out for me. Thank you. I was going to ask you to do it with the other hand. This is what happens when people are experienced. They just know what is coming next. So we are looking for mouth movements in Eric.

All right. I do not see any there. Go ahead, put your hand down. Eric, if I can have you open your mouth up for the camera, please. Good. At this point, you are going to be looking for tongue movements, jaw movements. Let me have you stick out your tongue. Perfect. And what you want to do is you want to do those two steps twice. So open the mouth and stick out the tongue as a two-step process. Do that twice.

By the way, those patients that see primary care do not have a lot of experience with psychiatry. When you ask them to stick out their tongues, every one of them opens wide like you are looking at their uvula. Eric, let me have you go ahead and back up for me. I am going to have you stand up. And if you could turn sideways to the camera, that would also be great. Maybe put both your hands out in front of you and just hang your hand down. You could let your fingers dangle there, too. So we are going to be looking for things in the torso, the trunk, other areas of the body as well. Good. Eric, you could relax your arms. Let me have you take a couple of steps. Excellent. You can stop. You can turn there. Good. So that is what we are going to be doing when we are looking for tardive dyskinesia. Go ahead. Come back over and go ahead and grab a seat. Thank you so much for that.

One thing I will also add, too, is if patients are making a tremor, if there is a tremor, there is a frequency to the movements. So it is not something that is interrupted. Like you see this, then it pauses, and then it does it again. If you see tremor, tremor is not tardive dyskinesia, and tremor is not to be scored on the AIMS examination.

AIMS Scoring and Interpretation

While we are looking at scoring the AIMS examination, we are looking at these seven body regions. The muscles of facial expression, which are up here around the eyes, the lips, and the perioral area. We are looking for pursing. We have the jaw. You can see that move side to side, anterior to posterior, laterally, and just chewing movements, grimacing, those sorts of things. You look at the upper hand, you can see the fingers, the piano fingers, and the guitar fingers. If you turn it over, you are going to look to see on telehealth: sometimes patients might rock, and rocking can be a little self-soothing, by the way. So if you see people move, two different directions when they are rocking, that can be a little bit more indicative. But we are going to be looking at our patients, and even on telehealth, we can get all of the body regions except for the lower limbs, by the way.

We need to know how to score the AIMS. When I first started, someone gave me a piece of paper and said, go do an AIMS on this person. And I was like, okay. I got a piece of paper, and I am like, I have no idea what I am doing. I have this AIMS, but I do not understand it. Here is how you score it.

Zero. That means there is no abnormal movement. It is just not there. No abnormal movement. That is a zero. If someone has a 1, a 1 means it is minimal. That might be extreme normal. So as you as the healthcare provider, if you are questioning whether or not that patient actually made a movement, that is probably going to be a 1. If you definitively know the patient is making some of these hyperkinetic movements, if you definitively know that is going on, that is at least a 2. And 2, 3, and 4 are going to be your mild, moderate, severe. And they are really going to be graded based on amplitude and frequency. So amplitude is the range of that muscle. Is it doing the whole range of the muscle? And is it doing that very frequently? If it is high amplitude, high frequency, that is going to be a 4. If it is low amplitude, low frequency, that is going to be a 2. And if it is somewhere in between the two, call that a 3 for moderate. I am not a huge fan of mild, moderate, and severe because we undertreat our patients that tend to be mild.

So in this particular scenario, how do we score the AIMS as well? So you can see in this particular pseudo-scoring that the lips and perioral area had a 3. The jaw had a 2. The tongue had a 1. What that is going to do when you add up the areas 1 through 7, that is your total score. And your total score is the added value of all of the individual scores. So 3 plus 2 plus 1 is 6. The total score there is going to be a 6. The severity score, there is an arrow that goes down here. That is your highest individual item score. Regardless of what you think it is, you might think, well, it is mild. Or you might think that it is severe or the patient is telling you how bothersome this is, and it is minimal movement. So they are telling you it is not bothersome, and they are high-frequency, high-amplitude movements. It is really based on the highest individual item score. Your severity is always the highest individual score. Just carry that down.

You can see in this case it was a 3 in the lips and perioral area. So it is a 3 for the severity as well. The other thing I want to say is too, when we are doing these activation maneuvers, we are looking for movements in our patients. If they appear during activation, just have alarm bells go off for you as healthcare providers if this actually bothers the patients. Please put that into your mental Rolodex.

Eric is going to take us through this patient case of Jeremy who, by the way, is not 58.

Patient Case: "Jeremy"

Eric Carlon: All right. So we have got Jeremy here. He is a 58-year-old man with schizophrenia. You have been seeing him for the last five years and treating him with oral risperidone, 4 milligrams. During his regularly scheduled appointment, you are performing an AIMS exam consistent with tardive dyskinesia screening frequency recommended by the APA. He does not wear dentures and has healthy teeth. He is right-handed. And when you ask whether he has noticed any involuntary movements recently, he says no.

So we are going to move through and watch some of these clips of Jeremy going through an AIMS exam.

Clip 1: Patient Walks Into the Office

This is your first encounter with the patient as they walk into your room. And you are already looking to see if you notice anything abnormal.

Clip 2: "Sit with your feet flat on the floor and rest your hands on your knees"

So he is being asked to sit with his feet flat on the floor and rest his hands on his knees.

Clip 3: "Open your mouth"

Now he is going to open his mouth, looking to see if there are any involuntary movements with the tongue.

Clip 4: "Open your mouth again"

And then open the mouth again. Times two. Same thing.

Clip 5: "Stick out your tongue"

Now we are going to have him stick out his tongue. Looks like something is there.

Clip 6: "Stick out your tongue again"

And then stick it out again.

Clip 7: "Extend your right arm in front of you and tap your thumb to each forefinger"

Now he is going to extend his right arm in front of him and tap his thumb to each forefinger. This is where we are going to be looking at his face. One of our activation maneuvers.

Clip 8: " Extend your left arm in front of you and tap your thumb to each forefinger"

Same thing with his left arm.

Clip 9: "Stand facing too the side and extend your arms in front of you"

And he is going to stand with his side facing you and extend his arms out front. This is where you are going to look at his trunk.

Clip 10: "Walk to the other side of the room and back"

Lastly, he is going to walk to the other side of the room and back.

Patient Case: "Jeremy"

All right. So we watched the videos of Jeremy. We are going to go through them again. And then this time we will try to pick up on some of the movements.

Clip 1: Patient Walks Into the Office

So right off the bat, walking into the room. You can see the jaw moving side to side a little bit. Nothing that you would see from the other side of the parking lot. But definitely some involuntary movements there.

Clip 2: "Sit with your feet flat on the floor and rest your hands on your knees"

So now he is going to be asked to sit with his feet flat and those hands dangling over his knees. And then we can look at his hands here, as well as his mouth and his face. I do not see anything too noticeable in the hands there, but you can still tell in the mouth.

Clip 3: "Open your mouth"

He is going to open his mouth.

Clip 4: "Open your mouth again"

Open the mouth again. You can see his jaw a little bit there.

Clip 5: "Stick out your tongue"

And he is going to be asked to stick his tongue out. See his fingers twitching a bit when he opens his mouth? Yes.

Clip 6: "Stick out your tongue again"

I will have him stick out his tongue again. That time you can see the tongue moving side to side. So it is that mild or moderate level of movement. So the differentiating factor to determine whether it is going to be mild or moderate is going to be how often it occurs. If it is something that is happening every once in a while or not necessarily repetitive, it would probably be more mild. If it is something that is occurring more frequently or a more persistent movement, then it is going to move more towards a moderate score.

Clip 7: "Extend your right arm in front of you and tap your thumb to each forefinger"

Now he is going to extend his right arm. We are going to do the activation maneuver. And then here you can look at his facial expression. And he is moving his other hand, too.

Clip 8: "Extend your left arm in front of you and tap your thumb to each forefinger"

He is going to do the same with his other hand. Yes, I think the mouth movement is probably the most noticeable.

Clip 9: "Stand facing to the side and extend your arms in front of you"

He will be standing and extending his arms out in front of him. See if we have any truncal swaying, rocking, leaning. I do not see anything there.

Clip 10: "Walk to the other side of the room and back"

And then the last one is going to be him walking from one side of the room to the other. So what do we think? Mainly just the mouth. A little stiff in the gait. So I think we have the hands. We notice some movement in the hands. Yes, mouth and the fingers. Yes.

AIMS Scoring and Interpretation

So that is that mild to moderate. And then the biggest thing, like I was saying, that differentiates the two of those is the frequency in which they occur. And that is one of the things with the AIMS is the mild to moderate is going to take precedent when you go down to score it, actually. I think it is easy to determine there is some movement. It is going to be something that is going to warrant further discussion and possibly treatment.

Any other thoughts on the AIMS? And you can incorporate really any types of movements that you are going to be looking out for. I do not know if there is a specific frequency that you would do that. But anytime that you are going to perform potentially an AIMS exam, you are going to be doing more detailed assessments of movements.

How do you know these are different from Parkinsonism movements? The biggest differentiating factor with the Parkinsonism-type movements is going to be the Parkinsonism is going to be more of a rhythmic-type tremor, whereas tardive dyskinesia is arrhythmic, involuntary. The other one, sometimes what you will have to do is assess for rigidity. With passive movements, you can have the patient sit, and then you can bend their arm at the elbow and see if there is resistance. And then also with the walking, the Parkinsonism, you notice more of a shuffling gait. Instead of going to the other side of the room and just turning around, they will shuffle and take six or seven steps to make that turn.

So is there a guideline that we should do this in all second-generation antipsychotic patients at least yearly, or if I am not noticing anything in mental status exam, I do not need to do one? If they are taking a second-generation antipsychotic, yearly is the recommendation. And then what would make it more frequent is going to be any of the risk factors that they might have. Yes, one a year is okay in that sense. And then you can also still do the unofficial AIMS, the unstructured exams to look for any involuntary movements.

Even if psychomotor activity is normal, do I need to fill out an AIMS? Depending on the risk that the patient has, you should be doing at least one a year.

If it is not bothersome to the individual, is treatment necessary? No, not unless it starts to affect activities of daily living, like we were talking about earlier. At least in my setting, the patients will sometimes start to struggle with feeding themselves. A lot of mine are walking, they use walkers, and they get this involuntary movement, the gait gets to be unstable, so it might. And then the other side of that is I have got patients that have dementia that have tardive dyskinesia and they cannot express how much it actually might affect them. So that is when it is going to be communicating with the staff and family.

So considering your own practice, how might you build tardive dyskinesia screening including unstructured monitoring and structured exams such as the AIMS into your routine workflows? You can type it in the chat. Let us know.

Jeremy, do you have any pearls?

Jeremy Schreiber: Yes, I do have a couple of pearls. Thank you for asking. I built the AIMS examination into my electronic health record. I own my own practice, and I handle some of the day-to-day or all of it. But I built the AIMS examination right into the EHR so I could do that. So one of the things that I do is I trend the AIMS examination with time. And I also, when I say with time, I mean I will have a special area where I document the exam. And then I also have a special area where I just write ancillary, and it is the AIMS exam. I do the same thing where I trend the PHQ-9s, the GAD-7s in patients that have depression or anxiety.

The other thing to note is that it is also a good idea when you are seeing patients if you are doing the review of systems and you are looking at musculoskeletal and you see the patient making these movements, I usually just document, hey, I noticed a jaw movement on 6-7, a lateral jaw movement, or I noticed this on whatever date it was because sometimes when I am seeing patients, I realized a long time ago that time passes differently for me than it does for them. And if I put the date in there and I let that continue to ride, what happens is what might feel like two visits for me could be four months or six months for my patients or two months, and it helps me trend how long this particular movement has been going on to make sure that I am very vigilant about catching it.

We have a lot of great stuff popping up in the chat here about noticing gait, posture, all of these things. I really liked what I have seen in the chat as we were running through this. I think we can look at some of these things. The baseline assessment, that is right, Geraldine, absolutely. And Debra has a really salient point here. Debra says, remember, these patients do not have to be taking antipsychotics currently, just have to have a history of use. So if people were taking them, and by the way, not just antipsychotics, any dopamine receptor-blocking agent. So other central dopamine antagonists can also cause tardive dyskinesia. Things like metoclopramide can cause this.

And I think Sheila, your point here about incorporating the regular assessment, exactly what I do. And if we are watching these patients regularly, Alana says we can put reminders into the calendars for our appointments. So all these EHRs work differently, but it is a great idea to do this because really the recommendations by the APA should be followed, in my professional opinion. I am not telling you all how to practice medicine, but I think if you put people on antipsychotics, you are probably looking at a comprehensive metabolic panel, a complete blood count, a lipid profile, you are doing an initiation, you are doing it for months, you are doing it yearly unless there is a reason that it is clinically warranted where we are doing it more frequently. So we are doing the recommendations, we just need to also make sure we are looking for movement disorders. Now by the way, I will also say that this webinar is about tardive dyskinesia, but we should be looking for movement disorders at large in our patients that are taking antipsychotic medications as well.

Evidence-Based VMAT2 Inhibitor Use

Jeremy Schreiber: All right, so let us talk about the evidence base for these VMAT2 inhibitors. For this section, I really hope to make you all comfortable with these medications, and the reason for that is because these patients really suffer, and I think that we have the ability to be champions for our patients with tardive dyskinesia. And a lot of times when I talk about tardive dyskinesia, I tell a story about a patient that I saw who had these significant symptoms and told me what I thought were insignificant symptoms. Her lips moved just a wee bit, and I did not really think it was a big deal, but the VMAT2 inhibitors came out, and she told me it was not a big deal. I put her on one of these medicines and then she is like, I am dating again. And I am not saying that you put your people on VMAT2 inhibitors and they become sexy and younger and live a vicarious life. What I am saying is that patients underreport their symptoms. As healthcare providers, we undergrade their symptoms, and so these patients are at a particular disadvantage to be recipients of treatment, and the VMAT2 inhibitors work well.

Patient Case: Judith

Anyway, let us start with a patient case here, Judith. Judith is a little bit more advanced in her years, apparently 12 years older than I am. She has bipolar disorder. She has been my patient for about 5 years, or your patient. She is treated with sertraline and lurasidone primarily to manage that depression. She takes an ACE inhibitor and a calcium channel blocker for hypertension prescribed by her primary care. Today she comes in, you see some sporadic blinking, and you see some mouth movements in this patient. And when you mention this to her, she says, "My husband has commented on this, these twitches over the past few months." So they are hinting at you right now that this has been going on for a few months. And she also says, "It makes me self-conscious," and the reason for that is because she does not usually realize the blinking or the mouth movements, and she does not know it until her husband calls attention to that. In other words, what is going on with you here? You are twitching, you are making this weird stuff. So she has got a level of embarrassment.

So on the AIMS exam, she shows mild orofacial movements, and by the way, mild is going to be a 2 on the AIMS scale. It resembles tardive dyskinesia. And when you do the activation maneuvers, the movements increase with the activation. So she, in essence, is probably hiding them, or she is not being activated or distracted. And she says that they do not interfere with her life or with her functioning, but really she is bothered by the fact that she thinks she looks strange. And this, I think, is a really consistent case with a lot of patients. I had a woman in my office two days ago, or I am sorry, last week on Friday, not two days ago, we were flooding. And she was doing mouth movements, and we started talking about it, and initially she was tossing it off, and then the more we chatted, she is talking to me about how she is not doing certain things like going to the store, this sort of stuff.

2 VMAT2 Inhibitors Approved for Treatment of TD

We are going to talk about these VMAT2 inhibitors for the treatment of tardive dyskinesia. There are two of them. So here are your answers. Deutetrabenazine and valbenazine. Those are the two answers. Both of these products serve as vesicular monoamine transporter 2 inhibitors. And what that means is they are reducing or preventing the packaging of the monoamines in the vesicle, which is subsequently re-released, so they work presynaptically by turning down the flow of dopamine. And if you remember, Eric said earlier that the theory here for patients with tardive dyskinesia is we have an upregulation of these dopamine receptors where they become hypersensitive. So if we could turn the flow down presynaptically, we can reduce the amount of dopaminergic signaling. And that is how these medications work.

So let us talk about these medications a little bit. We have deutetrabenazine. We have valbenazine. They are similar. They are both FDA-approved medications.

ARM-TD: Deutetrabenazine Flexible-Dose Trial

What is the efficacy data? Well, the efficacy data, when you look at deutetrabenazine here first, is that you have this reduction in the AIMS score over 12 weeks to a three-point drop. Now the patients in this particular clinical trial, this flexible-dose trial, their baseline AIMS scores were a 9. So they dropped by three points. You are getting down to a 6. By the way, there are seven body regions. So I do not know. Maybe it is a 2 in a couple of regions and a 1 in a region or two. The point here is significant reductions in their AIMS score. But I am also going to say something else important. Flexibly-dosed trials that are done by these companies are investigators have the ability to determine what dose of the product is working here. And if you look at the mean dose here, it is about 38 milligrams a day. I will tell you, as healthcare providers, I have talked to plenty of us, healthcare providers under-dose deutetrabenazine. So I am bringing that up to you that you get to real doses of this product when you are treating these patients.

AIM-TD: Deutetrabenazine Fixed-Dose Trial

Now this is your fixed-dose trial. What you can see here in red is that the deutetrabenazine 12 milligrams a day, that confidence interval really is not getting too much better than that of placebo in gray. Nominally, it is going to be better. But the two doses at 24 and 36 milligrams a day, those are going to be your doses that are really resulting in twice the AIMS reduction compared to placebo. These are, by the way, efficacious treatments. That is an efficacious treatment for tardive dyskinesia.

Long-term Data: Open-Label Extension Study of ARM-TD and AIM-TD Participants

They even looked at this data long-term for these patients in the deutetrabenazine studies. This is the longest study of a VMAT2 inhibitor to date at 145 weeks. We will call this three years. And what you can see happening over time is that AIMS score continues to go down. By the way, psychiatric patients are notorious. They are notorious for stopping medications in clinical trials. About 90% of the patients actually stayed on treatment for this. So it tells me that the medication is working and it is well-tolerated, or we would probably have a bigger dropout rate. At least that is my perception of what this data tells us.

KINECT 3: Valbenazine Fixed-Dose Trial

Now, what about valbenazine? Well, valbenazine is another FDA-approved treatment. Now, valbenazine comes as two doses, 40 and 80. These are six-week trials. One thing to note here is that valbenazine is efficacious at both 40 and 80. I am sorry I said something that is incorrect. Valbenazine has three doses, 40, 60, and 80. All of their doses are efficacious out of the gate. So you can start out right at 40 milligrams and be efficacious. The manufacturer actually recommends starting at 40 and after a week go up to 80, or you can choose 60 or stay at 40. It really depends on patient response.

Long-term Data for Valbenazine

This is looking at change in AIMS score by total study visit. Two different trials, one of which were rated by neurologists. That is where you see that four-point drop, both with the 40 and the 80 milligrams. The one on the right-hand side of your screen, this was rated by psychiatric providers, where you see nearly a 10- to 12-point drop in the AIMS score over this 48-week period of time. In both instances, when patients are taken off medication, their AIMS scores return. The point here is that these medications are not cures. They are treatments, but they are efficacious treatments where we can even oftentimes deliver amelioration.

Valbenazine: Change in AIMS Score (Open Label)

Here you are looking at the minimal clinically important difference in changes in the AIMS total score. What that is on the AIMS exam? Two points. You are looking at 90% of the patients plus in the valbenazine clinical trial had met the MCID. This is a really nice post hoc analysis of that KINECT-4 trial of those 48 weeks.

Prescribing Considerations

There are some things to note. The VMAT2 inhibitors do have some differences. They have similarities, both of which are FDA-approved treatments for adult patients with tardive dyskinesia. That is valbenazine and deutetrabenazine. There might be a posttest about that, valbenazine and deutetrabenazine. It might be deutetrabenazine and valbenazine, but those are going to be potentially a correct answer.

What do we need to know? In both cases, for patients that are over 65 with valbenazine, you do not have to do any dosage adjustments. With deutetrabenazine, they did not study a vast deal of this age group in their clinical trials, but they have plenty of exposure in these patients and clinical experience says there is really not a difference in terms of how we are going to dose this with patients who are a little bit more advanced in their years compared to others. Hepatic impairment, though, there is some separation here.

Deutetrabenazine is contraindicated, so if your patients have hepatic impairment at all, mild, moderate, or severe, it is not going to be for them. Deutetrabenazine is not your choice. However, with valbenazine, if it is mild hepatic impairment, you do not have to adjust the dose, but if it is moderate or severe, the maximum recommended dose for those patients is 40 milligrams. You do not have to do anything with renal impairment for either of these products.

Both of them can get away with using this medication with patients who are also on anticholinergics, but I will also add that anticholinergics can worsen tardive dyskinesia, so we really probably if we are using those to treat tardive dyskinesia, that is not what we should be doing. I would probably help get our patients onto the approved VMAT2 inhibitors and taper those patients probably off of the anticholinergic medications.

Valbenazine comes as a sprinkle. Valbenazine, though, goes both through 3A4 and 2D6, so if people are on strong 3A4 inducers, it is just going to chew up that valbenazine, spit it out, and patients are not going to get benefits, so it is not recommended. But if they are on strong 3A4 inhibitors, top line that out at 40 milligrams. Same thing with the strong 2D6 inhibitors, top it out at 40 milligrams. Now, deutetrabenazine, the dosing for deutetrabenazine is flexible. They have an array of dosages. Again, I really urge you to look at when you are treating these patients that you get to the therapeutic doses, so that way your patients can experience benefit. But with 3A4, we do not have any dosing recommendations that you have to do because deutetrabenazine does not predominantly go through 3A4. It predominantly goes through 2D6, so if people are on strong 2D6 inhibitors, again, that is going to raise the dosage of this. Just do not exceed that 36 milligrams, by the way, of the deutetrabenazine a day, 36 milligrams a day.

How about with food? With valbenazine, no recommendation. Deutetrabenazine comes as an extended release, so it is one tablet once a day, and with the extended release, it does not require to be with food, but if you are using the twice-daily dosing, which sometimes is appropriate, you do want to administer that with food per the package insert.

. If a patient has Parkinson's disease and is on an antipsychotic medication, how do you diagnose tardive dyskinesia when Parkinson's symptoms are similar to tardive dyskinesia, like the side effects of the antipsychotic? I am going to say something about this. Parkinson's disease and drug-induced Parkinsonism from antipsychotic medications present almost identically. You can see pill-rolling. You can see tremor. You can see the bradykinesia, like Eric said, the slowing. You can see the masked faces where they become expressionless. For lack of better terms, a melty face.

If someone has Parkinsonism or Parkinson's, they are going to have oftentimes the tremor. There is going to be a rhythm. There is going to be a hertz. If you can dance to it, it is not tardive dyskinesia. That will help you distinguish it. I heard a brilliant neurologist say if you can predict the next movement, it is not tardive dyskinesia. What she means by that is if you have 1, 2, 3, 4; 1, 2, 3, 4. If you were taking a video of that patient and you paused it and you turned it back on, it would still be 1, 2, 3, 4. Patients with tardive dyskinesia, though, you might see that, and then you will see a pause. Then you might see it again, or you will see an irregularity to the meter and the hertz, the frequency of movements for tardive dyskinesia is different.

We definitely want to get it right because if you think about Parkinson's or Parkinsonism, what that is a disorder of decreased dopamine signaling. If people have decreased dopamine signaling, they have decreased movements. If you remember, the mechanism of the VMAT2 inhibitors is to decrease the amount of dopamine. It decreases the signaling. Both of these medications that we talked about here have warnings to potentially cause drug-induced Parkinsonism. If we have a patient on an antipsychotic that has decreased dopamine signaling and that is due to the postsynaptic blockade so dopamine cannot touch there, these patients may have drug-induced Parkinsonism. Conversely, patients with Parkinson's also have decreased dopamine signaling. If we use a VMAT2 inhibitor, it could turn down that dopamine signaling even more, worsen it.

The other thing to note, though, is that if people have tardive dyskinesia and you use anticholinergics, they often have an inverse effect. They increase dopamine signaling, and that can worsen tardive dyskinesia. I hope that helps with how do we diagnose tardive dyskinesia if you are looking at patients that might have drug-induced Parkinsonism versus that might have tardive dyskinesia. If it is arrhythmic, which is without rhythm, I want you to think tardive dyskinesia. If it is with rhythm, I want you to think Parkinson's or drug-induced Parkinsonism. That would be two things to look for.

The other thing too with Parkinson's, you oftentimes can see some cogwheeling. Like with the AIMS, if they were in person, you would grab their arm, put your thumb right there into the antecubital space, and you are going to have that patient pull against you. If they have Parkinson's, you might see a cogwheeling. That is how that works. That is one of the ways that you do that.

Caitlin said, making sure that all staff are educated. I wholly agree with that, Caitlin. I had actually one of my staff members, my receptionist who has a degree in healthcare administration, was like, hey, can you take a look at this patient? I went and talked to my nurse and I said, oh, I almost brought you in to see this patient because I had tardive dyskinesia. This is like last week, I was telling you. A mild presentation. She said, oh, well, my one receptionist, my office assistant said, yes, yes. She recognized it. Like, hey, I think that patient might have tardive dyskinesia. It is really important. Yes.

And Johnny says, looking at gait, posture, this sort of stuff. Let us see what else we have here. A real patient example to walk through the AIMS assessment. It certainly would. I will tell you that the manufacturers of both of the approved VMAT2 inhibitors on their websites, they have videos where you can actually see real patients, not just people like me who are pretending to have tardive dyskinesia. All right.

Talking With Patients

How are we talking to our patients? Eric, can you help us out with this?

Connection Between Evidence-Based Medicine and Shared Decision-making

Eric Carlon: Yes, let us do it. All right. We are going to go over the connection between evidence-based medicine and then shared decision-making. And that shared decision-making is really you talking to the patients and trying to motivate them and encourage them to recognize that they might have something going on that they could potentially get treatment for. We see a lot of times these patients, if they buy into their treatment, they are more likely to be engaged and stay on that medication and continue it, really.

So really, it is always a risk-benefit assessment. You are looking back at the psychiatric condition diagnosis, the target symptoms, as well as their history and comorbidities, and then that shared decision-making. So it is a patient-centered approach, options with consequences, and then informed decisions reflecting patient values and goals.

Motivational Interviewing: Principles and Skills

So motivational interviewing. It is a style of dialogue between two parties, which is intended to motivate one party into making positive changes by compassionately challenging the status quo and helping them explore alternatives. So these principles being autonomy, collaboration, and then evocation. And then the skills that are necessary for this, connect with your patients and listen actively. You have to understand the patient's values, their fears, quality, skills, obviously being nonjudgmental, collaborative, challenging, flexible, empathetic, and then identify and work with the stages of change.

Use Shared Language to Reach Shared Goals

So using shared language to reach shared goals, that autonomy, collaboration, evocation, key aspects of collaboration, using shared language to describe the problem and how to approach it, art of communication, effective motivation.

The GAIN Model of Change Facilitation

And then there is that GAIN model of change facilitation. So goal setting, action planning, initiating treatment, and then nurturing that change. And then you have the stages of change there. But most importantly, I think it is just trying to have a conversation with your patient and trying to get them to buy into the treatment.

Patient Case: Judith

So we remember Judith. She is starting to notice these movements. What are you going to say to her?

Exercise 2

And you can script your discussion with the patient. How would you present treatment options? What key points do you mention about potential benefits and risks? How would you approach shared decision-making? And then you guys can, if you would like, you can type into the chat and maybe use sentences or phrases that you might help guide the conversation with Judith.

Jeremy Schreiber: You know, Eric, one of the things that I think about in this patient is the husband is saying stuff. Is anybody else noticing it? Saying to her these types of things.

Key Takeaways

All right. So let us talk about the key takeaways. Eric, that was a great close-out. If you noticed what he did there, he advanced the slide. That is some serious skill. And I will just give you some praise for that.

So really, what are the takeaways? The takeaways here are that if we have patients that are on dopamine receptor-blocking agents, think antipsychotics. That is the biggest bulk of these. These patients are at risk for tardive dyskinesia. The older patients are particularly at risk. We really should be vigilant. We should be screening our patients. We should be monitoring our patients. And this is not just like, hey, Jeremy thinks so. The APA has this. It really is best practice for us to be doing this. And I highly encourage you to look at these. The VMAT2 inhibitors are effective. They really are effective. And I will say as a psychiatric provider, sometimes I am not always in love with the effect size of these medications that I prescribe. And I want good treatments. And the nice thing about these VMAT2 inhibitors is that they really do tend to be effective treatment and help these patients with their movements, reduce those movements.

Compassion is where it is at. That is the other thing. Compassion, communicating well with our patients. I think if you talked to my staff, they would tell you that patients tend to like me. At least I think they do. I like to listen to my patients. And really what I want is I want to help my patients. I want nothing more than that. And I think if we spend the time and we talk to our patients, we can look at setting goals, we can collaborate, and we can really do well.

With all of that being said, I would first like to thank the moderators, the other faculty, Eric and Jayson, for joining me tonight. I would like to thank all of you out there for joining me tonight as well and joining Eric and Jayson. We are going to do a quick poll or two here, and then we will close it out and I will tell you how to get the credit.