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TMS Videos

TMS Review with Dr. Drew and TMS & Brain Health Founder Ben Spielber

By April 22, 2021April 26th, 2021No Comments
Neuromodulation

So this point, let me have you dispense with all that, let me get to my guest, Ben Spielberg. Ben is from the TMS and Brain Health in Santa Monica. Is that the actual name of the place to some brain health? Ben is a neuroscience and education master’s degree program from Columbia University. He focused on neuromodulation, which I think anybody knows me, know I’m obsessed with brain stuff and not just neuromodulation, but more particularly the non-pharmacological treatment of brain disorders. Would that be about right?

Exactly. And we’ll talk about some of that stuff. We’re also going to have Dr. Gary Donovitz in here a little bit later from BioTE Medical. You I’ve spoken to him before. I want to you know, this is a courtesy of our producer, Susan Pinski, who herself was misdiagnosed as depression went on the pellets, which is what Dr. Donovitz represents, and had a complete remission of her depressive symptoms. It was misdiagnosed. It was perimenopause, menopause, which can have mood and anxiety associated with it. That’s not that’s a symptom. That’s not the diagnosis. The diagnosis is menopause, perimenopause. Everyone missed that. One of the pellets, everything got better. So now she’s an enthusiast. We’ll bring Dr. Donovitz back and we thought was important to talk about it because there’d been some press on the palace recently. Controversy, is it good or bad? So we’ll get to that a little bit later in the show.

Also, we’re going to talk to a patient, right? Yes. So we are we’ve got a lot to get to. So first talk about let’s just to in general, you grew up in Los Angeles. Sorry, you grew up in Los Angeles. I did. And how did you get into neuroscience?

I got into neuroscience because when I was about twenty-two years old, I got a job doing neurofeedback as a technician in a drug and alcohol treatment. The click, click, click on the right. So click, click, click. So so what we would do is we would actually put EEG electrodes on people’s heads and we would we would connect those electrodes to a computer. And we tell the computer that when a person is exercising good brain activity to reward them in some way. So the screen would get larger if they were doing something good with their brain, whereas if they were doing something bad but saying these are brain waves. So we’re sort of assigning what’s good and what’s bad. But they were doing something bad, then the screen would get smaller or the volume would decrease. And over time they would actually learn how to volitionally control their own brainwaves, which would coincide with their symptoms getting better. Right

Now, now people get I did a couple of television programs on this topic where they had they had they were using actually fMRI up at Stanford for. Right. And people I couldn’t get the producers to get it right. Feel like, oh, I see. So you’re teaching them to be Zen and calm No, we’re not doing anything like that. You’re teaching them to get access to parts of their brain that are nonconscious, not at this point under volitional control and through a very complicated technology. Give them the feedback mechanism whereby they suddenly gain some mastery over that. Right.

About the way to say it. Exactly. Yeah. And with fMRI. So interesting, because what they’ll do is they’ll have people literally just look at a picture of their own brain and say, OK, you see this part, let’s change the color and let’s literally, you know, increase the blood flow to this area.

And everyone, my experience with these patients and I don’t have a lot, was they each one of them has their own sort of mechanism for activating this stuff. The study I’m talking about at Stanford was looking at a fireplace getting brighter and lower. It’s similar to what you’re doing.

And each patient would have a different they wouldn’t say, I’m going to make the fireplace. They’d think, oh,

I have little elves who are digging coal. They’d have very strange ways of accessing it from a standpoint of the image they would use to get to the brain functions.

It’s not like it’s not a direct process and it’s not. And that that was always the hardest part about when people first came in and they would say, how do I how do I make this move? How do I increase the volume? And you say, you know, it’s kind of just this relaxed focus that you have to have and you have to let your body figure it out. You figure it out. Everyone figures out everything. All right. So there you were. And then what happened? So I did that. I did that while I was studying psychology at Loyola Marymount University. And once I graduated, I realized that I really wanted more of the hardcore neurobiology. And so then I got accepted to the neuroscience and education program at Columbia where I really I kept doing the EEG research and I learned more about TMS. So while I was there, I got a job at a TMS center and I was actually originally hired to do neuroimaging before and after TMS

neuroimaging, meaning fMRI imaging, not fMRI. We were using EEG, we were actually using QEEG. So it’s (quantitative EEG’s), quantitative, quantitative EEG’s. So you create images out of that? Yeah, you create images out of it and. And it basically gives you these statistics once you record all of these electrode sites and then it tells you where each person lives in the general population, so so you may get a number that says this person has more of this type of brain wave in this particular spot than ninety-seven percent of the population or less than 90 or something like that.

It’s still very primitive interpretive biology. It is not a giant leap from for knowledge. I don’t mean to be cruel, but and I’ve seen some great derivative conclusions from quantitative EEG.

But it feels like, whoa, we should be able to have something, we

should have more. And the issue with it is that you end up if you do it right, you end up with so many different variables that it really takes so much energy to figure out what is actually going on there. Yeah. So in the clinic that I have now in Santa Monica, we actually don’t even use it because what I ended up realizing is I can I can figure out what to do with TMS just by talking to someone for their clinical response exactly their clinical sense. So talk about what TMS is and how it works. So TMS stands for transcranial magnetic stimulation, which is a mouthful. And it’s basically a device that can actually create a magnetic field, which basically turns on those brain cells.

So a reminder that when you have a magnetic field, currents run through magnetic field. So if you. I’m assuming it’s around the brain. Yes.

So we put a device on top of their head and then it focuses the field. And so the current is the current, which is electro biological, you know, shifts across cell membranes that transmit that electricity.

Exactly. Exactly. So neurons are there either on or off. And there’s been a lot of research with depression since the mid-90s that have shown that you know if you look at the brain of someone with depression and compare that brain or compare a brain of someone without depression, you’ll really you’re going to see the same pattern over and over again. You’re gonna see under activity in a specific part of the brain called the left dorsolateral prefrontal cortex. And so a TMS does is when it when it creates that magnetic field, we see increased activity in the left dorsolateral. What’s the thinking about what that region does? And it’s not doing a depression.

So it’s complicated. You know, that region alone, we know it’s associated with working memory, with executive function, with with a lot of the things that really make us human. Right. So so prefrontal cortex is the part in the front of your brain here. This is the part that develops in adulthood. Sorry for all the adolescents out there that we’re our prefrontal cortex, which you have to use because that part is kind of shut down, particularly in the males, and it’s broken into different pieces and there’s even some controversy on the anatomy. There’s a ventromedial prefrontal cortex, the dorsolateral prefrontal cortex, the I believe the insula is right in there against all that. Right. So orbitofrontal and orbital frontal, which maybe ties it all together, maybe. Maybe. Do you believe that? I do. I believe that, too. OK, good. So but the dorsal the absolute dorsal medial prefrontal cortex on the left is what we’re talking about. Dorsolateral prefrontal cortex (Yes yes), which is sort of here sort of and it is doing what it’s raising the chemistry there is doing. So I can’t imagine what that would be.

So so the lay explanation really is that there is this under activity in this area. We know it’s associated with depression and we see that as people get better with something like TMS, we see increased gray matter in that area. We see increased neuroplasticity. The real explanation is that there is really this complicated pathway involved. So you have the dorsolateral prefrontal cortex, which is connected to which is underactive. And there’s a very direct connection to a part of the brain called the subgenual anterior cingulate cortex

Subgenual anterior cingulate cortex So almost thalamic cortex. Very close. Very close. And so there’s in my experience, thalamus always gets into the conversation about mood and but no one knew why. Yes. So maybe we were just thalamus adjacent all this time. I It’s very possible. And it’s funny because this particular part of the brain, we really have no idea what it does other than every single study that looks at sadness in fMRI machines always has this particular area being overactive, overactive, (overactive), and underactive in the dorsolateral prefrontal cortex. Exactly. I’m guessing that it’s also overactive in 20 other things. In 20 other things. Where else? Just for just a few days.

But what’s interesting is it’s primarily sadness with this area. So so we know That this area is associated with an increased sense of sadness, but we haven’t actually found any other associations with it. We found just sadness, just sadness. Yeah, we found what? what we found that this area or that sadness has associations with some other areas as well, like increased activity in the amygdala. Right. So right. So my understanding, the amygdala, again, although it’s always going through incarnations, I just think of it as a salience center. It’s just acknowledging that’s important. Right. And so if you’re sad, a lot of stuff seems important to your brain that may be even isn’t important. Right. Right. It’s one of the problems with depression. You start obsessing about things and thinking about things and ruminating about your depression. That seems important. Right? Right. So it makes sense. Is that lateralize at all, too?

I don’t know. It’s interesting I’m not sure if that’s lateralized is it probably is to an extent.

And why do we and is it always on the left side and even left-handed, left-handed people?

So there’s switch. It switches in about 10 percent. That’s left-handed people.

Oh, let’s about how many left-handed people are truly left-handed, right? Yes, yes. Yes.

So the recall screener, my producer is truly left-handed. You can tell somebody really have to have by how they write. You know, we write like this left-handed people write like this right-handed person who write with their left hand right like this and they write sort of backwards. I do not know that little neuroscience, clinical neuroscience. But what you watch her do it. She’s said, my wife just does it this way. Like I was. I was. But she probably is. She’s kind of a lot of the a fair people are also sort of quasi ambidextrous, too. Right. So it doesn’t fully shift in the lateralization. Right.

And so TM’s so you’re creating her and that part of the brain, that dorsolateral prefrontal cortex, which probably boosts up the sadness in the center too right or decreases the activity center. Right.

So so one other, you know, major function of the prefrontal cortex, in general, is that it’s responsible for inhibiting all of these deeper brain structures so that, you know, these primal areas are not going overactive at times. When would when it would be inappropriate to write. Right. So that we know how to behave in a society.

Right. Right. Right. And then and then TM’s how reliable is it as an intervention.

So we get pretty good success rates. The clinical research tends to show about 60 to 70 percent response rate. I would say in clinical practice it’s a little bit higher because a lot of places know how to go off-labeling term.

Hey, guys, welcome back. That was extraordinary. For some reason, we’re not getting it on the screen here. Are we really back there? We are. OK, thank you for your patience. I don’t know. We have no idea what happened. We had a complete meltdown of all of our technology that we get for being so advanced here. I’m gonna pick up where we left off. We were talking about norepinephrine, serotonin and how these various chemicals, particularly in that region, are a are part of this story.

Mm-hmm. Mm-hmm. So we know that you know, antidepressants that involve serotonin selective serotonin reuptake inhibitors and Neuron Efferent and things like that work very well for some people. And I’m sure that as a physician dealing in mental health, you’ve seen that right. You’ve probably seen some people improve after a few weeks with know-low-dose SSRIs in a very dramatic way. But the research shows that 30 percent of people just do not respond to traditional antidepressants and talk therapy. So it’s clear that there’s really something else going on here that doesn’t just involve the traditional neurotransmitters and what’s and to be fair, we really.

We know a lot about what the antidepressants are doing. We really don’t know how they work. We don’t. We really just don’t. Yeah. And so that makes sense that we’d have some mystery around the non-responders exactly because we don’t know what the responders are doing either. So non-responders, 30 percent. And when you say in clinical practice, most of those people are non-responders. Those are the people that are slog through multiple medications. They’re adding the Abilify’s and the all the other stuff to see if there’s something mood stabilizers, (right) see if there’s something more going on here than just a depression. I mean, that’s sort of what psychiatrists are taught. Yeah. Now, in your recommendation, you would try TMS at that point, right?

Of course, yes. And actually and in other countries like Japan, for instance, TMS is actually recommended as a first-line treatment. So before anyone even tries medication, they would go to this temporary treatment that can have real long-term benefits.

Now, this shouldn’t be confused with electric shock therapy, which is a general activation of the brain. It’s trying to do the same thing, but it does it by causing a seizure. Exactly. So so electroshock or ECT really induces it creates this large electrical field that induces a seizure in the brain. And it does this multiple times. It involves anesthesia. There is sometimes temporary or even permanent memory loss. There’s confusion there. There’s cognitive fog. There’s really a lot of pretty serious side effects involved with it. Whereas TMS, instead of this really large electrical field, it’s really just a focused magnetic field without any of those side effects.

Right. I’m a fan. It’s expensive, isn’t it? A little expensive. It’s actually covered by insurance. So really that’s happening on the insurance company. You have to have failed other things, though, first. Right. Most insurance companies require that you failed anywhere between one and four antidepressants in the past for seems so silly. It does and then prior have to go to high doses and stuff. Exactly. Augmentation trials, things like that.

Let us take a ketamine call because this is also an interesting area of research. You know, something about and the caller’s name is Dylan. Hey, Dylan. Hi, yes, I’m 34 years old at inaudible Depression. I Just wondering about ketamine being approved by the FDA. So it’s like it’s covered by insurance because right now the only places that feel it are like out of pocket. Cash is like not doable for me to come up first security. Oh, hold on a little bit  (The taxability).   The Ketamine is available. There’s a nasal spray that’s available. Now, my question is, is that only After hold on second is that only after the infusion therapies that’s efficacious, you can use it as an individual therapy.

So as Ketamine or Provado, that’s the brand name, which is which is essentially half of ketamine was FDA approved in early. Twenty, eighteen. And we people use it instead of the infusions.

So I hope some people are using it after the infusion is sort of a maintenance thing. I don’t know if that’s just some senators are doing that. Probably

that may happen, but that’s not the indication for it. The indication is, you know, after someone has tried a few different medications, they can do the Esketamine nasal spray and they’ll come in. I think it’s twice a week for about a month. And then they figure out some sort of maintenance schedule. And because it’s FDA approved, it’s possible to get a single case agreement with insurance to cover it.

Have you tried that, Dylan. No, right, no, I’m not seeing any doctors I’ve given up on treating trying to get I want I mean, it’s complicated. I have very limited insurance right now. So or is there and I don’t I don’t know what kind of

dilemma started it up to you. I wouldn’t feel comfortable as a primary care physician prescribing that

right. And yet I often get in these desperate situations with people that don’t have insurance. They tried everything and I feel like I would like to.

Is there any intermediate way to get this medication without having to come in and see a psychiatrist and all that kind of stuff?

Not really. So so the only way to get Esketamine or ketamine infusion therapy is to either go to a dedicated clinic that focuses on this. So, for instance, TMS and Brain Health, we are going to start offering Esketamine. We have ketamine infusions that we do. But other than that, you know, it’s really up to the individual provider.

So I’ve seen some I’ve seen some striking responses from ketamine. I’m sure you have to. Yeah, right. People are just resistant as hell all of a sudden, three treatments and they’re like markedly better. What’s the mechanism? They suggest suspect there. Any ideas.

So we don’t know that much. We know something. So we know that, for instance, stress is a very big factor in depression and we know that whatever that means. Right. Right. So and when we say stress, that can mean, you know, it can mean developmental trauma. It can mean literally the current life stressors like work stress, family stress, things like that loss, loss. Great grief is. (anxiety) Yeah. So it’s all kinds of things. That’s why people say, what are we talking about? I’m going to bet I don’t know much about the mechanism, but ketamine is a dissociative anesthetic, so it literally disconnects you from it more effectively than an opiate, say, from horrible things. Right. And I’m wondering if that’s somehow helping people regulate their emotions. Well,

I think that’s part of it. And what we tend to see is that you know, very, very low dose ketamine like so low that you can’t even feel it. It doesn’t do anything. And there’s no therapeutic effect there. You have to somehow push into that dissociative state, even a very mild disassociative state, and then the therapeutic effect of that. It’s very interesting and I’m worried about it. And drug addicts, I’ve seen some relapses and people that work awfully well. And if I know real honest to God, drug addiction, if you give anything that is activating that reward set up, watch out and watch out. That’s the issue. Because with addiction, obviously, if you peel away the substance abuse, there’s almost always a mental health issue there. And so if it’s if it’s really this depression that’s causing the addiction, you know, you have to ultimately make that decision.

How does you guys do anything with panic attacks?

Not specifically, no. So panic is not something that TMS it helps with. I’m surprised.

We have people who will come in and they have depression and panic go together a lot. Yeah, they do. So so people will come in with depression and anxiety and panic and OCD and Pte you know what when we see people with these complicated things that then they tend to be better candidates and someone who’s, you know, they just have panic attacks. Right. That’s that’s really their only symptom. Yeah.

Although when you when people get better from panic attacks, they’ll usually look back and go, oh, I think I was depressed. Right.

So that’s me. That was my story. I had panic attacks in college and I was aware I wasn’t happy. When I look back now, I’m like, oh, I was profoundly different.

Yeah. Let’s see. I’m trying to get some calls here that are pertinent to why do we bring in

your case, your patient is your patient, your patient. Elizabeth?

Yes. She was a patient at our center. OK, and, uh, let’s maybe we should go to break or go to a break and we’ll bring Elizabeth in, and then we’ll bring Dr. Danovitz in later to talk about hormone therapy and its effect on mood. Be right back.

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I want to welcome Elizabeth to the program. Thanks for being here. Thanks for having me. It’s a pleasure. So how did you get to the point where you started contemplating TM’s?

Well, I was one of those cases that you were talking about a multiple failure on several different antidepressants.

How long had you been working, trying to get some sort of response? Oh, for decades. Decades, yes. And I imagine because I’ve seen lots of cases like that, I’m gonna to imagine you had periods where, like, it’s kind of working and then I would stop that kind of thing. Yes. Yes. Frustrating. Yes. And in my most before I started TMS, I was on a couple of different drugs are always added to the equation and I was getting better, but I was still depressed. So I had made some progress. But it was very frustrating because I couldn’t get all the way there because I do know what my undepressed brain feels right and bad out of fewer We get Ben on camera or not, but I’m going to have him sort of he’s sitting by here. And so this idea of complete remission is something that is becoming more, I don’t know, more anticipated, let’s say. I mean, I remember back in the early days of the SSRIs where, like when they’re feeling better, you know, but now those people should look forward to a true remission, resolute, sustained resolution of symptoms,

right? Exactly. Exactly. And with TMS, we’re seeing that about 50 percent of people are getting to that sustained remission, 50 percent of the recalcitrant cases. Yes. You were lucky enough to be one of those people. That’s correct. Did it happen fast or was it after only weeks of therapy or how did it work?

It happened fast and then a little bit over the course of the treatment. I was because of my experiences with not getting success with antidepressant therapy, the meds I wasn’t expecting very much. But in fact, the first day of treatment, I felt something activate in my brain. I was so excited about it. That’s literally what’s happening. Yes. So, yes, Ben showed me a picture of what the brain looks like when it’s not receiving blood flow to your course. Oh, yeah. So, yeah,

but I’m just asking how what are the ways that kind of help that if something like that happens during TMS. Oh you didn’t have right now.

Yeah that’s true. That’s true. No I not having a drink. Yeah. Yeah. So, so what we would do if someone, if someone seems like they’re going into a manic episode, is we would actually modulate some of the parameters of TMS. So we would either change the time, we would decrease the duration of each session or we would move the magnet to.

Of the medication not getting me to be where I wanted to be, mentally, emotionally, psychologically.

What did you think when you first heard about this?

I was scared. Like, what’s the magnet to my brain? Yes. He said, see if your insurance covers TMS. I said, what is that? It’s a transcranial magnetic stimulation. And I thought, I just have these pictures of these ECT’s in my head. But did this everybody please disavow yourself of all the movies you’ve seen about psychiatric hospitals? It does not apply to today. That is from 50 years ago talking about things that happened one hundred years ago. So although not that there were not egregious excesses by the psychiatric sometimes I think, you know, when people get very critical about psychiatry, that period when they were doing crazy stuff, they got a point. But that is long ago. Long ago. And did you think about ketamine? Was that something was presented to you? Also.

He did my psychiatrist did talk to me about ketamine, but he suggested TMS was the first thing that just got interested in this. Why would he have done that, you think? I

think TMS is more of a long-term solution, whereas ketamine, it works very well for some people very quickly, but it’s just not a long-term solution. You have to figure out some sort of menu. So so for somebody who has recalcitrant depression, you’re needing a longer-term solution than ketamine. Probably it’s. But still, those are the guys that get the ketamine of the recalcitrant guys.

I think I think people are more drawn towards ketamine. I think it’s a little trendy right now. And I think that there’s this idea that if something can work really fast, maybe I’ll just try that for I’ll try that first. And the schedule of TMS can be an issue for some people. So people have to come in five days a week for about six weeks. And then there’s also a six-session taper over the following three hours. (how does it take per session)

So that’s that’s really what we specialize in, is we do a three-minute TMS protocol. So teams used to take thirty-seven and a half minutes per treatment. And the FDA cleared a three-minute protocol last year, which basically uses a different frequency of the magnet pulsing to better enable the brain to learn it (got it), and if tell me we want to look into this at your center, where do they go? tmsbrainhealth.com

tmsbrainhealth.com

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