ECT Treatment: When to Refer, Who It Helps, and What Actually Happens with Dr. MaryEllen Eller

Dr. Eller

Greg, thank you for having me. From here on out, you can just call me Mary Ellen. Feels better.

Dr. Eller

Perfect.

Dr. Eller

Big picture stories. Number one, I love Dr. Pewter. I had the honor of being a first year resident while Dr. Pewter was my chief resident. We both trained at Loma Linda University for our psychiatry residency program. And I learned so many incredible things from the good Dr. Pewter. He loves all things psychotherapy. One of my favorite stories from my experience in residency is the program I trained and leaned heavily into psychodynamics.

It was in Southern California, so some psychoanalytic leanings as well. And Pewter loves therapy. And I went into psychiatry with the mindset that I was going to be really good at everything medication related. Loved the idea of psychopharm and all the things. And was determined that I was not a therapist. And somewhere in my third year of residency, I had a... One of the professors sat me down and had a conversation around, like, what kind of therapists are you?

What are we supposed to, you know, what should we be focusing on? And I flat out said, like, no, I'm not a therapist. I do meds. I love ECT. That's the kind of doctor I am. And they had a very point-blank conversation around, unfortunately, you already made the decision to be a therapist when you became a psychiatrist. And the only thing you get to choose from here on out is whether you're going to be a good one or not.

That did not come from Pewter, but Pewter after that laid the foundation of modeling how I choose to incorporate therapy into my patient interactions. And then he started a podcast and he let me be on it. So that was a lot of fun.

Dr. Eller

Yeah. All right. So other things you should know about me is I have a very goal-directed mindset. I love some degree of theory if it's applicable and useful. My program, we loved Myers-Briggs conversations. And what I learned about myself is my brain is wired for efficiency. I love doing things quickly. I have had to embrace the process of trying to shift into the mindset of being effective and not necessarily efficient.

And people like the good Dr. Pewter, his brain works very differently. And we had some lovely times as he was an attending physician and I was a lowly resident working underneath him. Where he would come to round in the hospital on a Saturday or a Sunday morning. And I would have a list of all the things I needed to do. And Cuter would sit there and want to talk to me about the theory behind just about anything.

Oh my God. Hours. And my soul would cringe because all I wanted to do was get things done. Once my list is done, I will talk about anything and I will be happy to do it. But I got to get the checklist done first.

Dr. Eller

And we've got to get through this list. I've got to write a lot of notes. So it was really lovely. I have been so, so blessed and honored just to watch... I've had a lot of really wonderful mentors and Dr. Pewter was one of them in his ability to find a way to balance meaning and purpose and to build a practice for himself that really incorporates the things that he finds to be most meaningful in his practice and is incredibly valuable to the clients that he treats.

And I think that's part of part of the wonder in psychiatry is that it is not one size fits all. And the world needs some of us who are Broad-minded, who want to think about theory, think through how problems develop, and really the psychological aspect of psychiatry. And the world also has a space for the more problem-focused psychiatrists who are checklist-driven, who want to have a problem, who want to see that problem solved, and then are more than happy to pass care on to someone who can carry it for a longer duration of time because we're built different and clients need access to a variety of different approaches for them to really be able to optimize healing.

Dr. Eller

One of the things I, again, I'm very grateful for. My program required all of us residents to have our own individual therapy. And it was mandated for at least two years. It was encouraged for all four. And I, of course, dragged my feet because I'm not a therapist. I don't want to be a therapist. I don't need a therapist. And I proudly finally went to my therapist and let her know, like, this is going to be the easiest hour of her week because I don't have problems.

And I am so grateful that my program set that as a requirement because I learned so much about myself, about how I process information and what my blind spots are. It also helped me become aware of how important information Being able to understand the value we assign to things, how that changes our language, how we approach problems, how we think through problems, and how we can sit with people.

Something that often comes up in supervision is that I prefer anger, which is a funny thing to say, but anger for me is an emotion that generates energy to get things done. That's not that I am incapable of experiencing other emotions, but in working with my therapist, we learned early on that while I experience other emotions, I very quickly choose to ignore them and choose anger instead, because anger allowed me to get things done.

And about a year into therapy, after claiming to have no issues and being a perfect, highly functional human with no issues whatsoever, My therapist had a beautiful balance of confrontation and asked me one day, if your daughter grows up to be like you, would you be proud? Stopped me in my tracks and we finally got to work and actually did some really good high quality therapy after that moment and worked with her for about three years.

Dr. Eller

Yeah, but it needed to happen. So now I can jokingly choose how I choose, joke about how I choose anger as my primary preferred emotion.

Dr. Eller

Yeah, one of my favorite things. Not a great segue after being like, doctor's angry. Oh, and she's an ECT doctor. Yeah, I want to, the, I,

Dr. Eller

No, let's just run with it.

Dr. Eller

I will hold you to keeping me on track. But number one, thank you for providing a place to have this conversation. ECT are letters that most people are aware of when they're put in that order and often come with a lot of emotion or a lot of opinion about what those letters mean. And the unfortunate reality is that ECT has a lot of stigma. It got stigma for good reasons.

It's also incredibly effective. It's incredibly safe. And it can be a very important tool that can alleviate suffering in the right population. And while I have had firsthand experience seeing the dramatic improvements that people can have in the process of getting ECT. I'll also be the first to say ECT is not the right decision for everybody. So to kind of understand that nuance, I think talking about the resistance or why people have fear or anxiety around ECT is probably the best place to start.

And to have that conversation, we have to kind of lay the framework of the history of how we came to start doing ECT in the first place. So number one, mental illness is not new. If we look back in the history of the world, for as long as people have been keeping records, there are records of humans who demonstrated the symptoms that we now call things like schizophrenia or bipolar disorder or depression.

We've labeled them different things across the years, but those symptom complexes show up across the life course of human history. And We really didn't have any structured way of understanding them or what to do with them. Enter the 1800s. Now we're starting to have more like psychological thinking. We're starting different schools of talk therapy. We're getting some structure around thinking about mental illness, trying to categorize and label things so that we can have shared communication between colleagues.

But we really didn't have anything beyond talk therapy. We had no medications. We had no interventions. We couldn't study living brains. So our best way of understanding why symptoms happened were brain injuries. If somebody survived, what was different about them? That's like the curious case of Phineas George. Or studying brains of humans who had died and trying to make conclusions based out of those ways of studying human behavior.

Which left us in the dark and taking some random guesses about what was causing these things. And we came up with all sorts of really creative explanations. Probably the most common theme was like witchcraft. Craft or possession seem to be a common thread across most of human history when it comes to mental illness. But as the study of mental illness or brain disease started to have more structure and we started having more shared language around how to describe these processes that we're seeing, we We came to realize that what we were doing wasn't doing enough for many people.

In the early 1930s, right, if you were diagnosed with something like depression and schizophrenia, bipolar disorder, the reality for most people is you'd be admitted to an insane asylum and you would never leave. Most of the time you would die within five to ten years, often with catatonia. There are Vivid case reports of the courtyards in insane asylums filled with waxy flexibility of catatonic individuals who died of exposure dehydration.

And well-intended people got desperate, desperately trying to help, trying to alleviate suffering when what we had available at that time, which was talk therapy, wasn't enough to talk somebody out of being catatonic. And we tried a lot of things. We got creative. Insulin came along and like woke up some kids. So we're like, ooh, let's try that. So we tried some insulin comas. We saw that humans who had epilepsy tended to have less depression.

So we tried some creatinine. Dr. Justin Marchegiani There are a variety of different stories around ECT came from, but by and large, the version of ECT that evolved into the form that we have today emerged around the 1930s, 1940s. I think the specific date was around 1938 and actually came from Europe where they were experiencing the same process that we were seeing in the United States. where if you go and get admitted to an asylum, you're likely going to die there.

And two creative guys, both of the neurologists, were out walking around the streets one day and they stumbled upon this profoundly psychotic individual. They bring him into the asylum and instead of using medication to induce seizure, They tried using electricity and over time fine-tuned the process of ECT. And that gentleman went from being floridly psychotic to being discharged to the community, which was unheard of. in those days.

There's not a lot of specific details around those case reports, but from that, we started to develop more technology of how to fine-tune the process. But again, in 1938, you don't have general anesthesia. You don't have meds. You don't have great ways of monitoring EEGs. We were living in the Wild West days of psychiatry, doing the best with what we had. And When many people think of ECT, that's what they still imagine the process is today, right?

Of like this incredibly inhumane process of some awake person getting electricity delivered to their head, having this incredibly heroic process looking seizure activity and then like losing their memory afterwards. Right. It's kind of how it gets depicted in movies. And if you've never seen ECT, it's easy to imagine that's what it looks like. When I was a med student, part of our third year clerkship experience was getting exposure to ECT.

And I I was like somewhere between nervous and excited. Right. When you're rotating in medicine and you're like in the emergency department and all of this, like you hear about seizures, but you never actually see them. Right. Like someone has a seizure, they end up in the emergency department. You do a post seizure workup. But it was very rare. I had never witnessed a an actual seizure event occur.

So part of me was really excited that I was actually going to see something. And I get to the ECT suite. And I sit there to watch my first ECT stimulus get delivered. Anti-climatic, so probably a correct word. Boring was more what I felt in the moment. Because at this point, the way that it's delivered, it's delivered using general anesthesia. So the human is fully asleep. Their body is fully relaxed with a paralytic.

There's no movement observed. The only way to know that a seizure has occurred is by monitoring with an EEG. We do inflate a blood pressure cuff to try and limit the paralyzing, that really profound relaxing medication from getting to at least some part of the body, usually the foot, so that we can preserve access to monitor a motor seizure. But overall, It's incredibly humane, it's incredibly quick, it's incredibly effective and it's nowhere as graphic as many people imagine it may look like in their mind because of how they've been influenced by movies like One Flew Over a Cuckoo's Nest.

Dr. Eller

I am excited for the day 10 years from now. I look back at how we practiced today and I get to say something along the lines of, oh, that was cute. They were doing the best they knew to do. The reality is back in the 1800s, the early 1900s, we had incredibly good intentions. I have to hold space to believe that that was true. And as we know better, we need to do better.

And I think that's kind of where psychiatry as a whole really has an opportunity to to accelerate our understanding of disease processes and what kind of treatment algorithms that we develop. From the 2000s, late 1990s, early 2000s and beyond, functional brain imaging became more widely available. But like truly prior to that, we had no real ability to study living brains in real time. So it truly has only been in the last 20 to 30 years that psychiatry has had an opportunity to start Widening our understanding of what's happening in a brain when they're experiencing the symptoms of depression or schizophrenia or what's happening in bipolar disorder beyond what our best guess is just based on the symptoms that we're able to observe.

And up until the last 30 years, within psychiatry, that's what we were left with, was trying to study or understand our disease processes by The subjective reports of individuals and what happened when we tried something, right? Which is where we came up with really creative ideas like depression must be a serotonin deficit because if you give the human a thing that increases serotonin, they feel less depressed.

So that must let through on. And as we've been able to study living brains, we've been able to understand that, yes, serotonin is impacted. But at best, serotonin is impacted as a much more downstream consequence of something else that is happening in that brain much higher up in the system. And for some people, modulating neurotransmitters can bring about significant symptom relief. But many people who try medications alone continue to have symptoms.

And so when that's the case, we need to take a step back and think through Where can we address these symptoms higher up so we can get closer to the root cause? I truly don't think we have any intervention at this moment that is a root cause intervention. The only place that I could start to argue with myself is in the realm of psychotherapy. In the way that psychotherapy can help address patterns and help modulate our stress response as far as how we perceive our environment, how we process information, and how our body physiologically responds based on how we process.

Beyond that, Our environment plus our genetics. So stressors as far as environmental factors, psychological factors, physical factors, plus our genetic predisposition is the simplest equation for why we end up with chronic disease processes. We don't have interventions right now to target genetics. We do have a lot of lifestyle strategies that can optimize our epigenetics, so we can have some power over the equation on the genetic side.

There are other things from the stressor side as far as environmental factors, physical factors, and psychological factors where we can start to modify Some stressors, but most people don't go around picking them up and choosing them. Most of the time our stressors are gifted to us. So we can't always control what stressors we're dealing with. But therapy at least has the ability to modulate how we process those stressors and how our body can respond to those stressors.

And when those things lead to disease, we need to have as many treatment options available and understand where those treatments interact with an underlying disease process. As far as I can tell, medications Target the most downstream effect from the consequences of that equation that we use in regular practice. If you start with targeting the most downstream consequence, it helps me understand why Dr. Justin Marchegiani And when medications have not been enough, then we need to find ways to target the system higher up in the process of that disease with the hopes of getting better results.

Dr. Eller

So my brain is very simple. So I have to come up with very simple ways when I read research and try to synthesize information in a way that makes sense to me. So I'm going to... I'll tell you how I understand or think about disease process and then share how that kind of spills out into my algorithm of how I work with patients. Because for me, I have to at least create in my mind a vision of what it is that I'm trying to do so that I can figure out how I can help.

So if we think about that simplistic equation of chronic stressors plus our genetics leads to chronic disease. The question becomes why, right? Why do chronic stressors, why do genetics lead to disease? I think the genetics piece, we can kind of table that. I hope that for many people, genetic risk makes sense as to why that might predispose somebody for a disease. It gives us insight as to why one family may have more depressive disorder while another family may struggle with things like schizophrenia or OCD.

All right. And while that can be an incredibly complex conversation, we're just going to leave the genetics kind of off to their self and say no more about them. Dr. Justin Marchegiani stressors may have pushed this human system to a state of disease. And when we think about environmental stressors, I grew up in Michigan. So the stories around Flint, Michigan and lead exposure and all of the significant impacts that has on brain health is something that sits close to my heart.

I grew up about 10 minutes from Flint, so I had a well. Oh, that might be one real simple. I don't know. But we can't take that part out of the equation, right? So if there are environmental stressors that are triggering or pushing our brain towards disease, we need to be aware of those. We need to address those. From a physical standpoint, we know that things like chronic pain...

Those things are stressors for our body, and they elicit a very specific chemical stress response. And psychological stressors elicit also a very prominent stress response. Slightly different in the acute phase, transitions to the more chronic stress response. So as I'm sitting with somebody, I'm listening for what are the stressors, what's the family history, what is the likely genetic predisposition that we're dealing with, and then what are the symptoms, what is the disease name that we're going to give this category of symptoms that they're coming to me for.

In the event, right, we've been living under chronic stress, the body's response to chronic stress releases chemicals that change how our brain and our body, how our cells interact with each other and how they communicate. In the brain, your brain cells, when they're healthy, should look like big, beautiful broccoli heads. Over time, chronic stress pushes those brain cells to start to look differently. And if you think of the chronic stress model, in my simplistic understanding, if you think of your brain as a company, the brain has a set budget.

And the brain can't just go around making more money. So when one department needs more money, it has to take it from somewhere else. For many people, that chronic stress response leads to increased staffing or increased demand in the threat detection department. And where it ends up stealing resources from are circuitry or areas in the frontal lobe. If you do spec scans or if you do brain imaging, you'll see that different disease processes map to different areas of increased activity and decreased activity.

Over time, when you have an area of your brain that is less active, as far as those beautiful broccoli head connections, if you're not using them, they take way too much energy for your brain to maintain them. So what we see over time is a decrease in postsynaptic or receptor density. The cells don't die, but they go from looking like these big, beautiful broccoli heads to sad, wussy asparagus.

Part of the medication process is that medications bind to receptors. So if somebody has been dealing with this chronic stress response for a long period of time and we put medications in a system that already looks like asparagus, if the medication cannot bind, it's going to have a limited ability to target or get that system back on board. Sometimes they work. Sometimes they can bind. The binding or the engagement of that chemical increases availability of the neurotransmitters.

More neurotransmitter over time can lead to that process of reengaging or increasing receptor density. Different medications work on different neurotransmitters. They combine presynaptic versus postsynaptic. They can sit in the cleft. They can work on enzymes. By and large, what we're trying to do is increase neurotransmitter to help increase density so that we can get healthy connection back. So what do we do if we're in asparagus mode and somebody has tried medicine and it didn't work?

When we look at trials like the STAR-D trial, what we know is that our first medication trial, regardless of what we try, has the highest likelihood of being effective for that individual. When we try our next medicine, and ideally we're going to pick it based on a side effect profile, we're going to use medical judgment to try and determine what medicine could be the best choice for them for their specific symptom complex.

But the likelihood of each medication trial treating someone's symptoms to remission goes down exponentially with each trial. And depending on where you look, those numbers could be anywhere with first medication trial having a chance on average around 30%, second trial around 20%, and by the time you're on your third medication trial, some studies are reporting a 5% likelihood or less of achieving symptom remission with medication alone.

And that includes medication switching. That includes augmentation strategies. And if you step back and you think about these big, beautiful broccoli heads that are now asparagus, it makes sense to me that I can put as many medications into that system as I want. If they can't bind, they're not going to be very effective. So as we've studied brains and we have learned more about brain circuitry and what circuits are influenced more strongly or are more impacted with certain symptoms, right?

And if we can map those circuits within a population, right? So one example of this is a lot of people with depression, right? We hear issues with sleep regulation, mood regulation, appetite regulation, focus concentration, rumination. And when we do large population studies, we have found that in that circuit, one area that we can reliably target and we can reliably map is is to the left dorsolateral prefrontal cortex.

Not the only area, but it's one that we like to talk about. And part of that is because it maps fairly well and predictably within a large population set, right? So in that treatment algorithm, if I've tried medications and I haven't gotten a significant symptom response, we haven't achieved symptom remission, my next question is, what can I do? How can I target something more upstream, right? So if the receptors aren't Aren't in a state where they can bind or respond to a medication.

Maybe I can bypass the receptor set and I can just directly stimulate that circuit using cool principles with like electromagnets and inducing currents. Part of what's happening is as neuroplasticity takes effect, as that circuit gets utilized, that receptor density increases, gets back to a healthier density, that circuit can maintain communication. Medications now have a better chance of binding. So oftentimes what we'll see is in the process of using things like neuromodulation, people who had been partial responders to medications previously or who were being prescribed heroic medication regimens can now have their symptoms maintained on a much more simplistic medication regimen.

And that goes back to this equation of stressors plus genetics leading to disease. If we can't do much to address the stressors and we can't do much in the world of genetics, then we need to do something to help protect the brain from going back to the state of disease. And for me, that's where medications are part of this chronic long-term conversation for a lot of individuals.

ECT is considered in that world of neuromodulation. ECT comes along and says, I don't care. ECT says, I am not going to pick one circuit. I am going to affect all the circuits. And that is the process of inducing a seizure. All right. So a seizure happens when all of the brain cells in your brain start talking at the same time. What we've learned in the process of doing ECT is that by repeatedly stimulating That brain activity, what we can see is widespread normalization of those areas of hyperdensity and hypodensity that come with that disease process.

Does that make any sense? Yes. I just realized I was talking for a long time. I used my hands a lot. It made sense to me.

Dr. Eller

So oftentimes we broach this conversation because we've tried medicine. Usually this conversation, we should start having it the moment we start medication trial number two, right? So someone comes in, they have a symptom complex. We prescribe a medication. We refer them to psychotherapy. They follow up. 2 months down the road partial response we've optimized the dose the moment we're having to start talking about a second medication trial or augmentation strategies is the right time to start laying the foundation of how these medicines are supposed to be helping what we expect what we're monitoring for to make sure that they're doing what they need to do and If you're not the 30% that gets remission with a medication alone, this is not the end of the road.

There are a lot of other and different ways that we can target the symptoms and get you relief. So starting the conversation early is really important. All of my patients, unfortunately for them, have to suffer through Eller's TED Talk to how their plastic brain understands why we get to a disease process as the foundation for the recommendations that I'm going to make. With that, I think a lot of people feel a sense of hopelessness.

Oftentimes when somebody is getting referred to me for ECT, the average number of medication trials is greater than 12. By the time they show up, they're feeling hopeless. They're feeling like this is the last stop on their journey, that if this doesn't work, there's nothing else for them. And... That paired with the frustration of every time I go to a doctor, they just give me another pill or they tell me to take more of it.

And for a brain, especially if we're talking about depression, oftentimes they're already feeling the sense of being a failure, being maybe not worthy of being helped. And that process of treatment and this constant cycling of trying new things, more things, oftentimes is easy for them to reinforce that thought process of I'm a burden, I'm a failure, I'm too much that goes hand in hand with the type of ruminative thoughts that we see in depression.

So I try to lay the foundation for my clients of why symptoms occur or my understanding of why symptoms occur. and what the pathway for treating those can be. ECT is also not the end of the road. There's all sorts of options beyond ECT if we go there, if it is partially effective or if it doesn't have durability for people. But perfect scenario is that the world of neuromodulation opens up for clients.

That conversation, it may get mentioned when we're starting trial number two because medication trial number two is ineffective. Medication trial number three, our likelihood of that working is less, and that's when we should be making referrals for neuromodulation. When we talk about ECT, I think highlighting that electroconvulsive therapy, the moment those letters or that word comes out of your mouth, I have seen a variety of reactions.

Yeah. Yeah. Oftentimes the individual with depression is desperate enough for relief that they are willing to sign up for just about anything. I have had to have some creative conversations around informed consent for individuals who had depression and were actively suicidal and they hear that under general anesthesia there's a chance of dying and that's their indication that they want to sign up. That's a bit of a red flag but also highlights the desperation that many people are in when ECT becomes part of the conversation.

My experience is that most of the time, at least in the world of depression, the human with depression is desperate for help. And often it's their support, the support around them, husband, wife, parents, that has the most resistance to the idea of doing ECT because they've heard that it's going to wipe out their memory, it's going to turn my loved one into somebody completely different. And so talking around the side effects, the risk benefits of ECT is critical to having that conversation.

Sometimes people bring up references to like one flew over a cuckoo's nest and how this is just incredibly inhumane and like the blight of psychiatry's existence. In those conversations, I will often kind of lay the foundation of the way ECT is done now looks nothing like the way that it was done in the 1900s. I often lead with humor, whether it's good or not. And I will often say something along the lines of how frustrated I am that my profession is still being held accountable for what we did in the 1900s.

But you're not going to your internal medicine doctor and yelling at him when he recommends an EKG because he used to flood let people and throw leeches on them, right? Yes, not fair. But oftentimes that's as far as that initial conversation goes. It's just laying the foundation of, yeah, there are good reasons why you're anxious about this. There's been a lot of misinformation. That misinformation didn't come out of nowhere.

This treatment looked real different in 1940. And it looks very different in 2026. Because of that, the side effects that people used to have in the 1950s and the 1960s is actually quite a different side effect profile than we have the way that we have fine-tuned the procedure now in 2026. The biggest resistance for most people is the fear around memory and memory concerns. Having explicit conversations around what those risks are is really important as far as an informed consent is concerned.

It's also really important for me that family is aware of what to look for because I may make adjustments in the way that I deliver the stimulus if they're seeing more short-term memory issues or confusion than I would consider to be normal in the process of doing ECT. Mm-hmm.

Dr. Eller

I'm going to try to be precise. Okay.

Dr. Eller

So things that respond incredibly well to ECT and poorly to other things. Depression with psychosis. Interestingly, the older you are, the better your response rates. And that's pretty unique with ECT. Bipolar mania, incredibly effective. It can also target bipolar depression, but the moment you have unipolar depression, bipolar depression, or mania and psychosis, ECT is incredibly effective. The other disease process that ECT has the biggest claim to fame in treating is catatonia.

Catatonia can be reversed. I've seen it reversed with as few as one ECT treatment. I've also seen it take longer, so it's one of the more unpredictable treatment courses, but it is the most effective way of treating catatonia. And in an ambulatory outpatient setting, the moment you see depression with psychotic features, especially in older individuals, That's a human that would be a really, really good ECT candidate.

Dr. Eller

So there's no absolute contraindication for ECT. However, anytime you have a seizure, you get a parasympathetic surge during the seizure itself. So your blood pressure goes low and your heart rate goes low. Immediately post seizure, you get a sympathetic Dr. Justin Marchegiani If you have an aneurysm, you may not be a good ECT candidate. I'm going to ask a lot of questions to make sure that those blood pressure changes are safe enough with your aneurysm history.

If you've had a heart attack in the last six months, if you have had a stroke in the last six months, we need to do some significant medical clearance. And usually if you've had a heart attack or a stroke, ECT is off the table for at least six months to give your brain and your body time to heal. Other things that are on the list of reasons to keep ECT in mind.

So pregnancy, especially if a pregnant female is experiencing mania or psychosis or depression that is putting her life and the life of her fetus at risk, ECT is effective and it is rapidly acting. The medications that we use to deliver ECTs, like the general anesthetic medications, they are generally considered to be safe in pregnancy. So in bipolar disorder, where the mainstay treatments like lithium and antipsychotics are Awesome.

What are the side effects? So generally speaking, side effects, anytime you're under general anesthesia, there are side effects that come along with general anesthesia. So headache, nausea, muscle stiffness or soreness from the paralytic agent, nausea as you're waking up. And you should be confused after you're coming out of general anesthesia, but that confusion usually lasts 15 minutes or less. From having a seizure specifically, seizure activity leads to The other specific side effect related to ECT is Dr.

Justin Marchegiani And I would expect short-term memory issues to linger for up to two weeks after your last ECT treatment. If you're in the midst of an index series and you're getting exposed to general anesthesia and having a seizure three times a week for four weeks straight, I'm going to expect some significant short-term memory issues. Now, what's really fascinating is depression itself has a profound impact on memory and memory consolidation.

Sleep as well has a significant impact in memory and memory consolidation. So while the risk of memory and short-term memory issues is something we keep a close eye on with ECT, When we have studied it across the population, over 30%, so between 30% and 40% of individuals who are in the midst of their index series have a better mini mental status exam score despite seizures and anesthesia exposure by their sixth treatment.

Now, that's not everybody. 15% of people have worse mentation. So it's not a zero risk. But In the process of informed consent, it's critical for people to know that doing nothing is a treatment option. They can choose not to treat their disease, but doing nothing and allowing a disease process to run rampant or run its course can have profound impacts, especially on memory, not to mention all the other downstream consequences of undertreated mental illness like depression, schizophrenia, and bipolar disorder.

Dr. Eller

Good questions. So the answer is a little variable depending on the disease that we are treating. So in a disease like catatonia, the answer is you're going to do ECT treatments three times a week until you're not catatonic. That might be one treatment. That might be 12. We're monitoring symptoms and we know that we're done with that Monday, Wednesday, Friday treatment course the moment your catatonia isn't recurring.

Depression is a much more standard treatment treatment treatment course. When I'm consenting somebody for ECT for major depressive disorder, I expect them to do 12 treatments. We try to do three treatments a week. Because this treatment is generally most effective in older individuals, some people have a harder time rebounding after anesthesia. So if they're having just profound tiredness, fatigue on the days between ECT, we can move it to twice a week if we need to.

But the sooner we get through that index course, the sooner they're going to start feeling better. So if we can maintain three a week for an average of 12 treatments for depression, then we're going to get through it in four weeks. And In depression, there's reported anywhere between a 60 to 90% remission rate, right? So the sooner we can get there, the sooner people can start feeling better.

But if we have to pull it down to twice a week because of side effects, then we can do that. Bipolar disorder is a little bit different as well. Typically, we treat whatever side of the disease phase that we're in, we treat to symptom remission plus three. So If somebody comes to me with bipolar depression and we start our index course, they're going to do treatments Monday, Wednesday, Friday.

And if at the end of treatment number six, they tell me my depression's gone, I'm feeling wonderful, I'm sleeping, I'm not hypomanic or manic, I'm just not depressed. Then we're going to do three more treatments Monday, Wednesday, Friday, and then we're going to convert usually over to maintenance. Similarly, in mania, we're going to treat it the same way. There is some concern, and it's hard to know if what we're dealing with is just And even more profoundly, is that most people after a manic episode, the majority of people who are coming out of a presogenic episode, that's their high risk period of time for swinging into hypomania or mania.

Majority will experience a depressogenic episode as they come out of that manic episode. So not 100% clear if ECT itself is a potential trigger for mania or the depressogenic side, or if what we're doing is just accelerating the healing process. And then the natural disease course is to swing from one to the other. So we're very cautious not to over-treat because we don't want to risk sending someone towards the opposite disease phase in the event ECT has the risk of doing that.

But we're going to monitor closely. Once we get done with ECT, the goal is to stay in remission. So typically what we'll do, I'll have somebody come back for maintenance treatment one month after they finish their index course. If no symptoms have recurred during that one month period of time, then we'll decide if we want to stay at one month. The one issue once we're in Amy C.

And I think a lot of that is that reflection of those chronic stressors plus genetic predisposition leading towards disease. And whatever we can do to optimize that equation, we can do that. You did ask as well, do people drive themselves to anesthesia or to ECT? And the answer is absolutely not. Anytime you're under general anesthesia, you may not operate a motor vehicle for 24 hours post-anesthesia. So ECT is not the right choice for people who are trying to actively work while getting treatment.

You can't drive yourself back and forth from work. I would expect you to be tired and have some short-term memory issues. So if somebody is actively employed and working, we often have to do to short-term disability or FMLA to get them time off work to protect their ability to do ECT. But that's one of the barriers as far as why ECT may not be the right choice for some people.

The other piece is you have to have resources in place for ECT ECT to be delivered safely. So you need someone to drive you back and forth to treatments. After anesthesia, you should have somebody like a responsible adult available to you if you have any issues. Not everybody has the luxury of having a friend who can drive them back and forth or who can stay with them 12 times in a month.

So those become very practical barriers as far as thinking through who ECT can be an appropriate intervention for.

Dr. Eller

If we need 30 more minutes to wrap up in a better way, you just let me know and find some time to throw it on us.

Dr. Eller

Bye Greg. Bye.