Deep Brain Stimulation: What We’ve Learned and Where We Are Going Next
Benjamin Walter, MD explores the evolution of deep brain stimulation and its role in shaping the future of adaptive, personalized neuromodulation.
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Deep Brain Stimulation: What We’ve Learned and Where We Are Going Next
Podcast Transcript
Neuro Pathways Podcast Series
Release Date: February 1, 2026
Expiration Date: January 31, 2027
Estimated Time of Completion: 30 minutes
Deep Brain Stimulation: What We’ve Learned and Where We Are Going Next
Benjamin Walter, MD
Description
Each podcast in the Neurological Institute series provides a brief, review of management strategies related to the topic.
Learning Objectives
- Review up to date and clinically pertinent topics related to neurological disease
- Discuss advances in the field of neurological diseases
- Describe options for the treatment and care of various neurological disease
Target Audience
Physicians and Advanced Practice providers in Family Practice, Internal Medicine & Subspecialties, Neurology, Nursing, Pediatrics, Psychology/Psychiatry, Radiology as well as Professors, Researchers, and Students.
ACCREDITATION
In support of improving patient care, Cleveland Clinic Center for Continuing Education is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.
CREDIT DESIGNATION
- American Medical Association (AMA)
Cleveland Clinic Center for Continuing Education designates this enduring material for a maximum of 0.50 AMA PRA Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.
Participants claiming CME credit from this activity may submit the credit hours to the American Osteopathic Association for Category 2 credit.
- American Nurses Credentialing Center (ANCC)
Cleveland Clinic Center for Continuing Education designates this enduring material for a maximum of 0.50 ANCC contact hours.
- Certificate of Participation
A certificate of participation will be provided to other health care professionals for requesting credits in accordance with their professional boards and/or associations.
- American Board of Surgery (ABS)
Successful completion of this CME activity enables the learner to earn credit toward the CME requirements of the American Board of Surgery’s Continuous Certification program. It is the CME activity provider's responsibility to submit learner completion information to ACCME for the purpose of granting ABS credit.
Credit will be reported within 30 days of claiming credit.
Podcast Series Director
Andreas Alexopoulos, MD, MPH
Epilepsy Center
Additional Planner/Reviewer
Ari Newman, BSN
Faculty
Benjamin Walter, MD
Center for Neurological Restoration
Host
Glen Stevens, DO, PhD
Cleveland Clinic Brain Tumor and Neuro-Oncology Center
Agenda
Deep Brain Stimulation: What We’ve Learned and Where We Are Going Next
Benjamin Walter, MD
Disclosures
In accordance with the Standards for Integrity and Independence issued by the Accreditation Council for Continuing Medical Education (ACCME), The Cleveland Clinic Center for Continuing Education mitigates all relevant conflicts of interest to ensure CME activities are free of commercial bias.
The following faculty have indicated that they may have a relationship, which in the context of their presentation(s), could be perceived as a potential conflict of interest:
| Ben Walter, MD |
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Glen Stevens, DO, PhD |
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All other individuals have indicated no relationship which, in the context of their involvement, could be perceived as a potential conflict of interest.
CME Disclaimer
The information in this educational activity is provided for general medical education purposes only and is not meant to substitute for the independent medical judgment of a physician relative to diagnostic and treatment options of a specific patient's medical condition. The viewpoints expressed in this CME activity are those of the authors/faculty. They do not represent an endorsement by The Cleveland Clinic Foundation. In no event will The Cleveland Clinic Foundation be liable for any decision made or action taken in reliance upon the information provided through this CME activity.
HOW TO OBTAIN AMA PRA Category 1 Credits™, ANCC Contact Hours, OR CERTIFICATE OF PARTICIPATION:
Go to: Neuro Pathways Podcast February 1, 2026 to log into myCME and begin the activity evaluation and print your certificate If you need assistance, contact the CME office at myCME@ccf.org.
Copyright ©2026 The Cleveland Clinic Foundation. All Rights Reserved.
Introduction: Neuro Pathways, a Cleveland Clinic podcast exploring the latest research discoveries and clinical advances in the fields of neurology, neurosurgery, neurorehab, and psychiatry.
Glen Stevens, DO, PhD: Deep brain stimulation is transforming the landscape of neurologic care, offering new hope and precision for patients with complex movement and neuropsychiatric disorders.
In this episode, we'll explore what we know and where we're going next. I'm your host, Glenn Stevens, neurologist, neuro-oncologist in Cleveland Clinic's Neurological Institute. And joining me for today's conversation is Dr. Benjamin Walter. Dr. Walter is a neurologist and director of Cleveland Clinic's Deep Brain Stimulation Program. Ben, welcome to Neuro Pathways.
Benjamin Walter, MD: Thank you. Thank you for having me.
Glen Stevens, DO, PhD: Ben, let's start by having you introduce yourself. Tell us a little bit about yourself, where you came from, your training and what you do here at the clinic. And I'm sure when you were a young lad back in the day, you never thought you'd have the title of director of the Deep Brain Stimulation Program.
Benjamin Walter, MD: Probably true, but I was always interested in the brain and neuroscience, so I might not have been surprised. I grew up in Philadelphia. I did undergrad and residency and fellowship all at Emory University in Atlanta with Mahlon DeLong and Jerry Vitek, both pioneers in the field of deep brain stimulation and understanding basal ganglia physiology. And came to Cleveland Clinic in 2004, and I've spent the rest of my life here in Cleveland in various capacities, but now back as the director for the DBS program and section head for movement disorders.
Glen Stevens, DO, PhD: Well, welcome. We're happy to have you as part of the team. I've been here about 35 years and I've really seen sort of the whole inception of the DBS program. It's been quite impressive over time with it. But for the audience out there, tell us what deep brain stimulation is and how it's evolved over the last quarter century.
Benjamin Walter, MD: So, DBS is a pacemaker for the brain. So it's very much like a cardiac pacemaker, except that the wires go into the brain instead of into the heart. The pacemaker itself is a battery in a computer that basically goes in the chest, very similar to cardiac pacemakers. They're a little bigger than heart pacemakers are now, but they're actually a lot smaller than they used to be and they're fairly small at this point. But that stimulation is able to adjustably control aberrant pathways and activities in the brain that are some of the underpinnings of movement disorders and tremors like Parkinson's disease, essential tremor and dystonia, and evolving to potentially be a treatment for other brain circuit disorders as well.
Glen Stevens, DO, PhD: How long does the battery last?
Benjamin Walter, MD: It depends. There's two major types of batteries, primary cells, which are basically like fancy lithium-based ion batteries, and they're good until they're done and then they have to be replaced. Those batteries will last depending on the settings and the currents that are used for up to five years or so. If it's really high settings, then it will last more like two, so it could be shorter. But there's rechargeable batteries now that will last 15 years, at least in most cases. And so for patients who need a longer battery life or at a higher parameters where that is more of an issue, we have rechargeables that really last quite a long time.
Glen Stevens, DO, PhD: And we certainly don't need to name the companies, but how many different DBS platforms are there? Are there two of them? Are there 20 of them?
Benjamin Walter, MD: Well, originally there was one, but now we have three. So with competition in the market, it's really great because in the last five to 10 years, innovation has really tremendously picked up in the neuromodulation space. And I think a lot of that is because of the competition and the additional investment in this marketplace.
Glen Stevens, DO, PhD: Yeah, I would agree with you. And talk a little bit about its initial use in Parkinson's patients. I was reading something where somebody was saying that the development of the subthalamic nucleus stimulation was paramount to levodopa being developed. It really just sort of was the fork in the road as Yogi Berra used to say as it went through. So tell us a little bit about its use in Parkinson's.
Benjamin Walter, MD: Well, there are a number of things that were going on when DBS was first thought of, and actually the first instance was by mistake, as most things are.
Glen Stevens, DO, PhD: Serendipity.
Benjamin Walter, MD: And yeah, neurosurgeons in France actually, Illum Lewis Benevitt, who was one of the early pioneers in DBS on the neurosurgical side, was working with central tremor patients to make a thalamotomy or a lesion in the brain. And they test stimulation before they make the lesion with the lesioning probe and somebody had the gain turned to the wrong, the 10X instead of the 1X. And so they got a hundred plus hertz instead of like 10 hertz, which would've been good for test stimulation. And the tremor went away. And so they realized that that was a reversible way of doing it. And at the time, palatotomies were being done or lesions in a globus pallidus internal segment for Parkinson's disease, but it was known that there's some limitations with being able to do that bilaterally without affecting speech in patients with Parkinson's disease. So they thought, well, maybe we could use this in that instance.
And at the same time, at Emory, Dr. DeLong and Thomas Wickman were working with the animal models for Parkinson's, which Dr. DeLong, who was my mentor, did pioneering work, got the Lasker prize in medicine for really discovering the circuitry in the brain that underlies Parkinson's and Huntington's and things like that. And with that work, they were looking at the subthalamic nucleus with subthalamic lesions and were able to show that in the animal model that that was effective in Parkinson's. So they put this together and Dr. Benemic came up with the idea of doing STN stimulation or high frequency stimulation for Parkinson's. And that's really where it took off. And then it spread to other targets, including the thalamus, which is where it really started for tremor and GPI of the globus pallidus internal segment for dystonia as well.
Glen Stevens, DO, PhD: Other indications for DBS?
Benjamin Walter, MD: So, there are other indications. So dystonia I just mentioned, the indication is for a generalized primary dystonia, so not caused by an insult to the brain. Even for pediatric patients as young as H7 could be candidates for that. And it's quite effective for those patients. It really changes lives in a positive way. It's also approved for obsessive compulsive disorder, which is a small indication. It's not a large population of people that are candidates for that that meet the stringent criteria, but it is effective for that and has been shown to be. So also for refractory epilepsy as well has an indication, but there's a lot of potential indications that are being explored or sometimes done off label, and that space is really dramatically expanding.
Glen Stevens, DO, PhD: So, my guess is you're pretty good at brain anatomy, but the lesioning or the stimulation is based on where you assume something is anatomically, right? Or you go by a plate or a map.
Benjamin Walter, MD: That's where it starts. Yeah.
Glen Stevens, DO, PhD: That's where it starts. And you can then stimulate and then you need to look for a response, I assume, to decide, am I in the right spot? Or tell me how you do it.
Benjamin Walter, MD: Yeah, that's correct. So the MRI, which fortunately gives us a fairly fine resolution, as you know, the brain and these basal ganglia circuits is a good first way of estimating where you want to stimulate and you can find the structure on an MRI, but the MRI then has to be fused to a frame which is attached to the patient's head in most cases. And usually a CAT scan is taken of that combined situation and those images are fused. There's error sometimes infusion and that can cause errors. And then when surgery takes place, the surgeon makes a bur hole and the CSF can leak out a little bit and there's always a little bit of brain shift and that will change the location of everything as well because it's based off the initial scans. But even if you're hitting the spot that looks right on the MRI, you're not necessarily in the right spot.
And so the real proof is what is there? What does it sound like? Can you pick up the neural activity of that region? And then even more so test stimulation either with a test probe or more importantly with the final DBS probe when you place it in there, does it do what you expect it to do what you want it to do? And so that can be refined to microns in measurement to really get the right location and make sure that you're getting benefits without untoward side effects.
Glen Stevens, DO, PhD: So, you're playing name that tune with the neurons?
Benjamin Walter, MD: Pretty much. It's like traveling through Europe and listening to different dialects of different languages and making sure you're first in the right country and everybody's speaking Spanish and Spain, but then finding the right dialect for the right city that you want to be in.
Glen Stevens, DO, PhD: So how specific is that?
Benjamin Walter, MD: It's very specific.
And so we know the anatomy very well in the physiology for the regions that we're accustomed to looking at, but you can certainly tell the difference between a white matter tract, which is fairly quiet and gray matter, which has different types of neural activity, but each area has different types of neural activity. It changes in certain ways. And even more so when you stimulate, it has predictable effects. And even with that, the anatomy is somatotopically organized. So organized along the homunculus or the shape of the body and the brain. And that also will tell us even more precisely where we are within that region, within that subregion in the brain.
Glen Stevens, DO, PhD: So, it would seem well suited to some type of AI process to help identify the waveforms or the sounds, those types of things. Are you utilizing that? Or you guys can tell it's not going to add much to it?
Benjamin Walter, MD: You can tell. It's more than just listening. And certainly there are folks that have developed some, at least machine learning driven programs to recognize the physiological patterns and give some predictability to what you're listening to and where it is. And is this characteristic of a subthalamic cell or not? Kinds of questions and putting it all together is really integrating that with the imaging, the expected trajectory, the stimulation effects that you're getting in that patient as well. So it's a lot of other things. Nothing's been done at that level using any type of computer aided algorithm, but certainly people I think are looking at it.
Glen Stevens, DO, PhD: Outside of movement disorders, what areas are you most excited about for DBS?
Benjamin Walter, MD: Outside of movement disorders in the near future, I would say depression has been looked at for quite a while, even from the beginning days of when I started at the Cleveland Clinic. I've been in some cases where we're doing DBS and clinical trials for depression and different targets. So seeing that is quite amazing to see somebody's mood change at the flip of a switch like that, but it's taken a long time to get that right and perfected because it's such a heterterogeneous population with diverse causes and exacerbating factors in the circuitry has been proven to be different for some of these different types and causes of depression. But that is being worked out. And I think we're at the point now where there's a lot of promise in finding subpopulations of people with depression where DBS can be very effective. And so there's clinical trials starting right now looking at DBS for depression again.
Benjamin Walter, MD: And the other area I think is really promising, and this is being pioneered at no other than the Cleveland Clinic here in Cleveland, Ohio by Andre Machado is DBS for post-stroke recovery. And that has, I think, a lot of promise as well, and it's exciting.
Glen Stevens, DO, PhD: Yeah, we've had them on talking about that. It's very exciting area, very exciting. Talk about adaptive DBS.
Benjamin Walter, MD: Adaptive DBS is one of the newest technologies and capabilities, and it's really the tip of the iceberg. What we've been doing with DBS thus far is fairly simple, even simple compared to what cardiologists have been able to do with cardiac pacemakers, in part because the brain is such a complicated organ and it's more difficult to design, improve effectiveness with that level of complexity. Adaptive DBS is tracking brain signals that correlate with disease states. So we can listen to the physiology or pick up the oscillatory activity in a target like the subthalamic nucleus and Parkinson's disease where it's mostly being used and the beta band oscillations correlate with the severity of Parkinson's symptoms at any given time. So high beta is suggestive of uncontrolled Parkinson's symptoms. And when it goes down, the patient generally has better symptom control. And you see those changes with medications, for example, when the medications kick in, beta goes down.
And so we can track that, and that can be a control signal for adaptive DBS. And so what has been done is showing that if you do that, and there's a couple different ways of doing it, but I think the more simple example is, as beta goes up, it hits a threshold and the stimulation is going to go up and bring the beta down. And as the beta goes down, at some point the stimulation will then go down. And so you keep this more even level of symptomatic control, which is really important, particularly in Parkinson's disease, where the DBS is actually adapting and personalizing to the individual patient's symptoms, not just in general, but at that moment in time in their life, what they need at that time is what is ideally being delivered.
Glen Stevens, DO, PhD: And is this a hardware issue, a software issue? So let's say I have a DBS in and something great gets figured out three or four years down the line, are you going to have to exchange the probes?
Benjamin Walter, MD: Yeah, so it's both, and it depends. It depends on to what degree. The technology currently depends on all the software and the hardware and the IPG, which is the implantable pulse generator, which is basically the battery and the computer that's the pacemaker in the chest. That's what drives it, but that gets replaced periodically. So that's an easy thing that will periodically get upgraded. And then the software on that device gets updated much more frequently because it can be updated wirelessly and there's different features that can certainly be unlocked in any of these devices over time. For it to work well, you ideally want leads and connections of those leads, the connector wires to have very good signal isolation properties so that you can get good signal to noise recording from the lead, which the older ones aren't designed to record, they're just designed to deliver stimulation.
So their signal denoise and recording aren't as good, but they still work in most cases. So some of the early studies with this were with the older legacy leads, and now they have directional leads out with newer NASA design technology to really isolate the signal noise so you get even better recording from these, and that works better. So somebody with very old leads might be able to do this if they have the right kind of leads that could plug into one of these newer batteries, and it may not work quite as well. And the most ideal state is getting all new stuff, but we wouldn't at this point recommend anybody change out their leads just to get adaptive DBS. Usually there's other reasons for doing that if that's going to happen.
Glen Stevens, DO, PhD: So, I guess we're going to go a little bit deeper on directional leads here since you brought it up. The way that I understand this, and you could tell me if I'm wrong, is the directional lead, the benefit of it versus the conventional lead, the conventional lead gives more of circumferential stimulus, so there'd be more risk of side effects by affecting tissue in adjacent area, and the directional lead would be more in a perpendicular axis. So it would give you more pinpoint treatment, less risk of negative side effects. Am I saying that any way that makes any sense?
Benjamin Walter, MD: Yeah, that's more or less right. I mean, essentially when you have four levels of stimulation up and down the wire, which is what the older leads would have, typically you have four different spots in the anatomy along that trajectory that was chosen to put that wire in. So you're kind of fixed with that vector to be able to have choices for stimulation, but it still gives you some adjustability by being able to pick one or multiple contacts and arranging your stimulation around that. But the directionality of that is really up and down and you don't really have much flexibility to adjust the current in the XY direction or perpendicular to that wire. And in the newer directional leads, the typical configuration is those two middle levels are split in thirds with different contacts facing different directions, anterior and posterior, medial, and posterior lateral ideally. And so now you can then turn one on in those segments at a time and be able to push the current forward, backwards, left, or right.
And actually a lot of them can actually do that in a graded way so that you can more or less control that vector of stimulation in the XY space, whatever angle from the lead that you want to go out towards, you're going to push out in that direction. Now in general, it's going to still take more of a spherical form to some degree, but it's going to be biased in that direction. So it's not 100%, but you do get to shape that current in that way. And now we can turn on all these different contacts to different degrees and really be able to shape that ball of current. So it fits just tightly within the structure that we want to stimulate, which has various different shapes and sizes, and it isn't spilling out or spreading into neighboring neuroanatomy that causes side effects.
Glen Stevens, DO, PhD: So, DBS seems good at treating tremor, dyskinesias, not so good at treating freezing gait and some of the other problems. Is that going to be something you can overcome or you got to look at a different direction for that?
Benjamin Walter, MD: Well, both. I think you have to look at a different direction, but I think hopefully it can be overcome. Freezing of gait is a real challenge. I think in part because it's a heterogeneous problem with regards to this underlying circuitry of it, I think there's different circuits probably involved in the brain, different areas of pathology that may affect it. And sometimes freezing of gait response to levodopa, for example. And so those patients that have a dopamine response of freezing generally respond to DBS because DBS is modulating that dopamine responsive motor circuit in the brain, and a lot of those patients over time, they may lose a response to levodopa, and they typically would then also lose the response to DBS. And a lot of patients never have a response to either one to begin with. And so as it evolves and gets worse, it gets harder and harder to treat freezing of gait. So the question is, what other parts of the brain are involved in. Is there a node or a circuit that will unlock that freezing so that patients can move and walk more freely and get their independence back? And that is the holy grail for gait treatment and Parkinson's disease.
Glen Stevens, DO, PhD: I’m confident in you. So it sounds like less dopa responsive disorders, less likely to work with DBS, is that right? In terms of like PSP, does progressive supranuclear palsy DBS help that or not help it?
Benjamin Walter, MD: No, it doesn't. So when you're in the circuit that's being treated for Parkinson's disease, we're typically in that basic ganglia thalamocortical circuit, which is really modulated by dopamine. And so yes, the dopamine responsive disorders typically respond those that don't. So you've got your atypical Parkinsonian syndromes like PSP or multiple systems atrophy that have Parkinsonism, but they don't really respond to levodopa in most cases. And probably what's happening there is with regards to levodopa is that there's post-synaptic damage as well. So it's not just the dopamine cell that's degenerating, but it's downstream parts of the circuit as well. And I think for DBS, it's also part of that extension of the anatomy is affecting different areas within the circuit. So we're also not able to capture or modulate the circuit because it's broken in other places. So people have looked and looked at other targets for some of these things to see, again, if we can find a node that would work for those symptoms that doesn't work, that isn't a typical node or part of the circuit that would use for Parkinson's disease, but that has also been elusive as well.
Glen Stevens, DO, PhD: So, let's say you put a DBS in me. How long does it take to sort of get me where I am functioning at the level? Is it right away? Is it a week? Is it a month?
Benjamin Walter, MD: Well, for different reasons, it takes a little bit of time and sometimes it can take a little longer. We usually wait several weeks, usually about four, just for things to heal up and-
Glen Stevens, DO, PhD: So you just turn it off?
Benjamin Walter, MD: It's just not turned on yet. So it's planted, but some patients will have a decent amount of benefit just placing the wires. It makes it very hard to fine-tune and find the best settings if it already looks different or better than it was before. And that's due to local edema around the lead that goes away in a short order of time. And so once the patient is then stable and kind of back to their normal state, we can start programming. And people that are more complicated with Parkinson's and have dyskinesia, for example, we're often balancing stimulation with meds, which have similar effects, but the stimulation is more durable and 24 hours a day. But if we're stimulating the subthalamic nucleus, which will cause dyskinesia as we get benefit, just like meds do, we're then going down on meds going up on stimulation. And we do that gradually to get the right balance and also so the patients tolerate that medication reduction. And so we typically do that over several visits and it'll take several weeks from one visit to the next and then usually a couple visits. So within a couple months, we have the meds down and the stimulation is turned up and it's controlling their symptoms.
Glen Stevens, DO, PhD: And can the patient alter the stimulation or you have to do it?
Benjamin Walter, MD: To some degree, yes. There's millions and millions of different settings that we can set. So there's a lot of parameter space that's complicated for us. It would be insurmountable for a patient to explore. And so what we do is we find the best place to stimulate. We find the dose of stimulation in that area that seems to help, and we go up and find where the limits of that is. And usually we're going to set things fairly conservatively, but as we know where they're at and what they tolerate, as we become comfortable with that patient, we can give them a range, usually the amplitude between those different settings so that we start out at one place, but maybe between visits, they can go up a little bit. And maybe if they have side effects when they go home that we didn't see in the office because they were very subtle, but become apparent as they live with them for a little while.
It's like walking out of the shoe store with the shoes and seeing if they really fit or not. Then if it doesn't feel right, the patient can turn it down a little bit with their patient controller. And typically we'll also, if we're doing iterative programming in their second session, we'll give them their first session settings as a backup and likewise as we go along. So they always have an easy way to go back, roll back time to a month ago and be on those settings if that was truly better for them.
Glen Stevens, DO, PhD: And what developments or challenges do you see shaping the future of DBS at this point?
Benjamin Walter, MD: Well, this is a technology driven high science area, so it's rapidly progressing and it's somewhat unlimited. I think that what we're sensing, the data that we're getting from the brain is fancy, but fairly rudimentary still at this point. That's going to get a lot more complicated where we can get different signals from different parts that may have different meaning. We can integrate that information. I think you're a little limited with more fancy technology like machine learning and AI, and that there's a lot of unknowns in controlling that, but even already there are some algorithm-based programming options that are becoming available. It's not exactly machine learning or AI, but a step below that, but much more predictable. And as we evolve through these things, I think we'll get to more computer generated ways of digesting all this tremendous information and coming up with solutions that can be tested and then changing it over time with the signals.
The data that we get out of the signals, it's really simplified in several different ways and that helps everybody know what we're actually looking at and be able to respond to it, but there's a lot more information. We're looking at frequency plus or minus five hertz within the beta ban usually, and that's the band that's the control signal, the amplitude of that itself. But there's so much more data there that has important meeting and as we get a better understanding of that, that's going to be the control. Looking at multiple things at the same time, again, it'll get a lot more complicated and a lot more computer controlled.
Glen Stevens, DO, PhD: Ben, fascinating stuff. Final takeaways for our audience?
Benjamin Walter, MD: Well, I think this is a really exciting area. It was when I started it more than 20 years ago, and it just gets more exciting every day. So it keeps me coming to work in the morning, plus I get paid. So it's a lot of fun.
Glen Stevens, DO, PhD: Well, we appreciate your joining us and look forward to all the great things you guys are doing. Thanks a lot.
Benjamin Walter, MD: Thank you. Thank you for having me.
Closing: This concludes this episode of Neuro Pathways. You can find additional podcast episodes on our website, clevelandclinic.org/neuropodcast, or subscribe to the podcast on iTunes, Google Play, Spotify, or wherever you get your podcasts. And don't forget, you can access real-time updates from experts in Cleveland Clinic's Neurological Institute on our Consult QD website. That's @CleClinicMD, all one word. And thank you for listening.
Neuro Pathways
A Cleveland Clinic podcast for medical professionals exploring the latest research discoveries and clinical advances in the fields of neurology, neurosurgery, neurorehab and psychiatry. Learn how the landscape for treating conditions of the brain, spine and nervous system is changing from experts in Cleveland Clinic's Neurological Institute.
These activities have been approved for AMA PRA Category 1 Credits™ and ANCC contact hours.