Spinal Decompression and tPRF Therapy
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Webinar Transcript: Transcutaneous Vagal Nerve Stimulation and tPRF Therapy

Dr. Freddys Garcia:
Hello everybody. My name is Dr. Freddys Garcia, and today we’re joined by Dr. Adam Klotzek. We’re doing a webinar on the topic of transcutaneous vagal nerve stimulation.

We’re going to be talking a lot about that, and at the end we’re going to discuss how the Stimpod NMS460, and its application of transcutaneous pulsed radiofrequency, can make vagal nerve stimulation even better.

Before we do that, I want to tell you a little bit about Dr. Klotzek.

Dr. Klotzek has been very generous in sharing his expertise with us on various topics, and everybody is giving us amazing reviews. So Dr. Klotzek, everybody loves learning from you.

Dr. Adam Klotzek:
Well, thank you. I appreciate that.

Dr. Freddys Garcia:
If Dr. Klotzek is new to you, he is a DC and holds a Doctor of Chiropractic degree from Logan University, along with his neurology diplomate status.

He is an accomplished worldwide lecturer in the field of neurology and neurological treatment, delivering over 700 presentations, totalling over 11,000 hours of education on various topics.

He has over 25 years of clinical experience in the trenches, and he has attended to over 12,000 patients, treating them for a multitude of neurological and non-neurological conditions, including, but not limited to, concussions, vestibular disorders, chronic and acute pain conditions, headaches, ADHD, neurodevelopmental disorders, scoliosis, sports-related injuries, and more.

He has a special interest in developing novel treatment applications, an interest in the effects of joint misalignments and manipulation on brain function, and he has also authored a number of published research papers.

When he is not busy studying, learning, and being a clinical consultant, he loves music, playing the guitar, fine dining, fine wine, reading, personal development, and spending time with his close friends and colleagues — which I’m lucky to say I’m one of those people.

Dr. Adam Klotzek:
I feel fortunate too. Thank you.

Dr. Freddys Garcia:
Welcome to another webinar, Dr. Klotzek.

Dr. Adam Klotzek:
All right. Thank you, Dr. Garcia, for that gracious introduction. I’d also like to thank Algiamed for giving me the opportunity to share information about vagal nerve stimulation.

As a lot of you know, vagal nerve stimulation is the “in vogue” thing to be doing with patients with a whole bunch of different conditions — and with good reason.

Dr. Freddys Garcia:
Which I think you’re going to share with us.

Before you get started, I’m going to jump off the stage. I can tell you’re ready and raring to go. I’m going to jump off the digital stage. I may come back if I have a pressing question or if somebody has something really pressing in the webinar chat. Then I’ll be back at the end to do a little outro with you and some Q&A, if there are any questions.

So the digital stage is yours, and I’ll see you on the other side.

Dr. Adam Klotzek:
All right, thank you.

We’re going to spend some time talking about vagal nerve stimulation. Obviously, we’re not talking about the invasive kind, where doctors go in and wrap coils around the vagus nerve. That’s not really within our scope.

We’re going to talk about the non-invasive kinds, and more importantly, we’re going to talk about transcutaneous vagal nerve stimulation.

For those of you who don’t really know me that well, I’m kind of a “why” guy. I’ve always been intrigued by the why of how things work. Why does this happen? Why do you get results when you do this? I’ve always thought that if you can answer the why, you can automatically develop the how — or how to change things if they aren’t working the way you want them to work.

So we’re going to spend the next half hour or so going over the why of transcutaneous vagal nerve stimulation. At the same time, we’re also going to talk about the different technologies that have been used and studied. We’re also going to talk about why one technology may be better than another, and so on.

Just to give you the lay of the land, we’re definitely going to talk about some neuroplasticity concepts, the history of neuromodulation, and pertinent clinical anatomy of the vagus nerve. We won’t go into a lot of detail with that because we don’t have enough time.

Then we’re going to spend more time talking about mechanisms of action. How does this actually work? Why are clinicians seeing the results that they’re seeing with vagal nerve stimulation?

More importantly, we’ll talk about why pulsed radiofrequency is something that really intrigued me from hearing various doctors talk about the results they’re getting with pulsed radiofrequency.

We’ll emphasize that. We’ll also look at what conditions can be treated, or what has been shown in the literature. We’ll talk about how to stimulate the vagus nerve, whether there is a difference between sites, which site may be better or worse, contraindications, treatment parameters, and then we’ll spotlight the difference between DC galvanic stimulation, which is one of the stimulation types, and pulsed radiofrequency.

Hopefully, we’ll summarize things and everybody will enjoy the information they learned.

Let’s start with neuroplasticity.

Neuroplasticity is also the “in vogue” thing. People are talking about the brain these days and how we can change the brain and make it work better. There are techniques out there that are brain-centric, focusing on making changes in the brain, and vagal nerve stimulation plays a role in that.

What I want you to understand is that neuroplasticity consists of two main concepts or ideas.

The first is neuromodulation. I put DC galvanic in parentheses here because one of the ways you stimulate the vagus nerve is by using a DC current. It has been shown that DC galvanic stimulation seems to focus more on the neuromodulatory effects for nerves. That means it is more of a functional change that happens in the nerve.

You can either make the nerve work better, which is long-term potentiation, or make the nerve work worse. But really, it involves delivering an electrical stimulus over the nerve, as well as using pharmaceutical agents — which is not really part of what we do, so we’re not going to talk about that.

But I want you to understand that in order to neuromodulate a nerve, you need energy. The nerve needs energy. The nerve needs ATP. It needs to produce more transmitters, vesicles, and so on.

That is going to become really important when we start distinguishing between the two main stimulation types: DC galvanic stimulation and pulsed radiofrequency stimulation.

Pulsed radiofrequency is more involved in the neural remodeling part of neuroplasticity. This is really important. These are the actual structural changes that happen within the axon, the synapses, the neurons, and the myelin sheaths. You make more synapses, more axons, the myelin sheaths get thicker, and you get more mitochondria in the cell bodies.

These are actual structural changes. Obviously, they influence function as well, but this also requires energy. It requires ATP, and I’m pointing that out because it will become important a little bit later in this presentation.

A lot of technology has been developed as a result of electrical stimulation: cardiac pacemakers, spinal cord stimulation, and transcranial magnetic brain stimulation. They all work on the same basic principle.

Let’s talk a little bit about the history of neuromodulation.

I found this interesting when I was putting this seminar together and going through the literature. I do want to let you know that there are probably about 40-plus contemporary articles supporting what we’re talking about here. It took me some time to put that together, but I think it’s worthwhile.

Let’s start at the beginning.

In ancient Egyptian tombs, if you look at their hieroglyphics, there are drawings of catfish. What’s interesting is that the Nile electric catfish produces electricity. So why were they spotlighting that in the tombs of the pharaohs?

We also have accounts from ancient Greek times where they used torpedo fish, which are basically electric rays. They can produce voltages of up to 225 volts. These rays were used to treat various painful conditions.

There’s one story where a man was walking on the beach and presumably had gout. He stepped on one of these torpedo rays, got shocked, and his gout was cured. He didn’t have any more pain in his foot.

So you can look at these rays as being the first portable electrical stimulators. There are a lot of historical references to them, but the idea is that electricity, radiofrequency waves, and related energy forms do affect our bodies.

Then Galvani came around and discovered that nerves work based on electricity. Then we had the development of the battery, circuits, electromagnetic induction, and eventually the first electrical therapy devices.

Because of all these inventions, we got pacemakers and implantable devices. But during that time, there was another lineage of literature and experiments using a different frequency range — in the 500 kHz area.

The first accounts of radiofrequency use were back in the 1970s, and I’ll talk more about that. Then it developed into the use of pulsed radiofrequency later on.

Then we had the discovery of the inflammatory reflex, and that was a game-changer. The discovery of the inflammatory reflex made people say, “Oh, this is why these devices work.” That started a whole string of developments.

Eventually, we got into vagal nerve stimulation, and then transcutaneous pulsed radiofrequency stimulation as a therapy.

To summarize some of the historical events: in order to develop this idea of electricity and the use of electricity to treat people, we had to dismiss Descartes’ idea of the nervous system.

Descartes thought nerves worked like plungers, with fluid in the nerves. The idea was that a plunger would physically move fluid in the nerve and cause limbs to move. That idea eventually didn’t hold up.

Then Galvani came around and showed that if you complete a circuit by having a rod touch two different metals, you can make a frog’s leg contract. A copper coil was attached to the nerve, the connecting rod touched the metals, and the frog’s leg moved.

Then we had the battery discovered and many other developments. All of this led to the development of these devices that we already talked about.

Now let’s talk about another arena: the use of a higher frequency range, around 500 kHz. I think the historical development here is very important.

The first accounts of radiofrequency use were back in the early 1970s, where researchers discovered that if they exposed a nerve to a 500 kHz waveform, it would cause thermocoagulation. That started the whole idea of radiofrequency ablation for the treatment of different conditions.

In the 1980s, they discovered something interesting. The application of constant radiofrequency ablation to distant nerves also yielded positive results in the area involved in pain or another condition.

So people started trying to understand why the application of a coagulating thermal stimulus that damages a nerve would improve a condition not directly related to that nerve or level. That started the conversation about neuroimmunomodulation.

It suggested that radiofrequency waves were doing something more than just thermal coagulation.

Then in the 1990s, researchers proposed pulsing the radiofrequency instead of applying it constantly. That became known as pulsed radiofrequency. You have an on-and-off application.

They found that it was a good alternative to constant radiofrequency ablation, but with pulsation, you don’t cause the same kind of damage. So then they had to ask: why is this working?

In 2008, they found that intra-articular pulsed radiofrequency was also very effective. Before that, they thought you had to touch the nerve with the probe to create the effect. Later, they found that you didn’t have to do that.

So again, they had to ask what was really going on and what these treatments were doing.

Then in 2013, which is really interesting, researchers started doing intravenous pulsed radiofrequency using the cephalic vein. This produced positive systemic effects.

There’s one account of a physician with lung cancer who went into remission. There are also accounts of people with depression and other disorders doing well with this type of therapy.

The thing I want you to get here is that pulsed radiofrequency treatments can have a systemic effect on function within your body — not only on nerves, but also on other structures.

To me, that’s really intriguing. From a clinical standpoint, it suggests a very powerful positive effect that we can leverage.

In 2015, researchers eventually discovered that they didn’t actually have to cut the vein and insert the probe into the vein or directly touch the blood. They found that pulsed radiofrequency waves easily cross over the wall of an artery or vein.

That led to the development of transcutaneous techniques, which is what we are seeing now and what you’re seeing with the Stimpod. It was a very interesting progression in how they got to that point.

Now we need to talk a little bit about the vagus nerve.

One of the important things to understand is that about 80% of the fibers in the vagus nerve are afferent. Only about 20% are efferent. That means the majority of what you’re doing when you stimulate the vagus nerve is sending information centrally.

Where does that information go? It goes to a major area called the nucleus tractus solitarius, or NTS.

The NTS is very important because it projects to other central brainstem structures. One is the locus coeruleus, and another one is the nucleus raphe magnus.

The locus coeruleus is involved with noradrenaline and noradrenergic integration. The nucleus raphe system is involved with serotonergic activity.

If you look at the output of the locus coeruleus, it starts to shed light on why vagal nerve stimulation has far-reaching effects outside of the site where you’re stimulating.

You can affect the cerebellum, which is involved with movement. You can affect the amygdala, which is involved with emotions. You can affect wakefulness, attention, the prefrontal cortex, behaviour, anxiety, depression, and sensory processing.

So you have a wide range of areas that are influenced by output from the locus coeruleus, which is driven by output from the NTS, which is then driven by vagal nerve stimulation. That is very interesting, and it helps explain why we see the things we see.

Remember, I’m a “why” guy, so I think it’s important to understand that.

The locus coeruleus doesn’t just project to the brain. It also projects down into the spinal cord. That means it can influence motor control, sensory function, and pain control.

You also have efferent fibers, and I’m not dismissing these. They originate from the nucleus ambiguus and the dorsal motor nucleus of the vagus nerve. They project to cardiac, respiratory, and visceral organs.

So you will have an effect directly on those organs, but understand that you’re also going to have a significant effect on other systems due to these central projections.

Let’s look at the therapeutic goal. What are we really trying to do with vagal nerve stimulation?

I think I’ve hinted at some of these things, but basically, you’re trying to create inflammatory homeostasis. If you think about it, you could say inflammation is at the root of many diseases, which is not too far out there based on what we’re seeing in the literature.

You want to restore balance. When inflammation gets out of control, the output of the dorsal motor nucleus of the vagus and the vagal centres may not be able to control it. Stimulating the vagus nerve has the ability to restore balance using a more non-local neuroinflammatory mediating process.

A lot of this was discovered in studies done with sepsis. Rosas-Ballina and colleagues, in 2009, described how brain signals via the vagus nerve reduce inflammatory cytokine production and improve survival in sepsis models. That contributed to the idea that vagal nerve stimulation can help create inflammatory homeostasis.

You also can’t talk about vagal nerve stimulation without talking about the cholinergic anti-inflammatory reflex.

Immune cells produce cytokines. These cytokines stimulate the afferent fibers of the vagus nerve into the central autonomic networks. You then get an output that causes an increased amount of acetylcholine, and that acetylcholine helps stop cytokine production.

If you look at this in a very simplistic manner, if you have a problem with this output, you won’t be able to mitigate and control inflammation. That is part of the why behind vagal nerve stimulation. It is a very good way to increase the output of these fiber systems to mitigate inflammation.

We also have the benefit of neuroimmunomodulation. We achieve this not only through the cholinergic anti-inflammatory pathway, but also through the hypothalamic-pituitary axis and the splenic sympathetic anti-inflammatory pathway.

You have three systems working together, driven by the integration and stability of the NTS, to help modulate inflammation.

We all know inflammation is normal. We need inflammation in the body. We need it to heal. It becomes a problem when it becomes chronic, which is what we’re seeing a significant increase in throughout society. We could have another discussion as to why that’s occurring on another day.

Here’s another important point. These cholinergic fibers being stimulated from the brainstem also go into the spinal cord. They go into the dorsal horn. What they do there is block the primary and second-order neurons associated with pain fibers.

We already know that with nerve injury, neuropathy, and neuropathic pain, cholinergic tone is decreased. These fiber systems are not working as well. They have found that if we simply increase the amount of acetylcholine, we can induce analgesia.

So now you have vagal nerve stimulation as an adjunct to treating different pain conditions, which we’ll talk about.

I’m amazed by the wide usage that this type of therapy can have and the impact it can have on a person. It is a good tool to have.

What are the treatable conditions?

Let’s run through these.

POTS — believe it or not, vagal nerve stimulation improves POTS. It also improves mood. A lot of people with POTS are depressed, and many are anxious.

How does it work? We already talked about that. With vagal nerve stimulation, you activate the locus coeruleus pathways, changing brain activity and prefrontal activity. It reduces sympathetic pacemaker activity in the brainstem.

The rostral ventrolateral medulla is a key centre to remember. It activates the sympathetic system. It’s part of pressor responses and vestibular activation. But it is regulated by the caudal part of the ventrolateral medulla.

So the caudal ventrolateral medulla inhibits the rostral ventrolateral medulla, which decreases heart rate. Then you have vagal outputs through the celiac pathway and to the spleen, reducing cytokine production.

That’s pretty interesting.

Post-stroke rehabilitation is another area. With vagal nerve stimulation, you can have a neuroprotective effect on nerves, promotion of angiogenesis, and protection of the integrity of the blood-brain barrier. It also reduces cortical spreading depression.

For those of you who may not know what that is, cortical spreading depression is a process where neuronal activity in the brain gets depressed and then spreads over non-vascular territories. In other words, it’s not just confined to the distribution of the middle, anterior, or posterior cerebral arteries.

The mechanism is a little complex, but it doesn’t involve direct vascular integration. That’s important because cortical spreading depression has been implicated in primary headaches and migraines.

So yes, this is relevant to primary headaches and migraines.

Vagal nerve stimulation can modulate pathways that decrease activation of the trigeminal nucleus. That’s important. It can also modulate autonomic function, trigeminal neurons, cortical spreading depression, and nociceptive modulation.

If you have headache patients and you’re treating headache patients, it makes sense to perhaps incorporate vagal nerve stimulation as part of your repertoire. It’s not going to hurt them, and as we’ll talk about, there is very little downside to it, with a lot of upside potential.

Low back pain is another area.

There was a study by Helmy in 2023. They had a control group that just received exercises, which a lot of us use. Then they had the intervention group, which received exercise plus vagal nerve stimulation.

The parameters used were 25 Hz, with the pulse width and intensity based on patient tolerance. They gave the treatment for 20 minutes a day, five times a week, for two weeks, on top of exercises.

One group just did the exercises, and the other group did VNS plus exercises. The group that received VNS with the exercises did significantly better. The mechanism appears to involve the anti-inflammatory cholinergic activation and the effects in the spinal cord on pain fibers.

Epilepsy is another area.

It has been known for over 30 years that vagal nerve stimulation helps with epilepsy. It’s been around for a long time.

One study in 2021 looked at cortical networks involved in epilepsy. They measured network activity prior to stimulation, then during stimulation, and then after stimulation. During the stimulation, the network stabilized significantly.

This instability is thought to contribute to epileptic attacks. During stimulation, the network became more stable. When the stimulation was removed, there was a return toward baseline, but in 30% to 50% of subjects, the effect persisted for an extended period of time.

So vagal nerve stimulation can help stabilize brain networks.

Cardiovascular disease is another area.

The studies done on this mostly used low-level transauricular stimulation protocols. They used an intensity probably around 50% to 80% of the stimulus strength that reduces the heart rate.

What you do is ramp up your device until you notice the heart rate decreasing. You can do that a couple of ways. You can use a stethoscope to listen to the heart, or you can use a pulse oximeter. I think it’s probably more accurate to use a stethoscope because pulse oximeters have a delay between the actual measurement and the displayed reading. It’s not a big delay, but in a pinch, you can use a stethoscope.

What are the treatment benefits? It suppresses atrial fibrillation, alleviates post-myocardial infarction effects, helps with ventricular arrhythmias, and helps with ischemic reperfusion injuries. It also improves diastolic parameters in heart failure, particularly in cases where left ventricular ejection fraction is not impaired.

The mechanism is thought to be the restoration of a favourable sympathetic-vagal balance.

COVID-19 is another area. Studies have shown that vagal nerve stimulation can benefit COVID-19 patients. There is significant literature regarding respiratory effects and the ability of vagal nerve stimulation to help with those.

It protects against infection, attenuates acute lung injury, and improves lung function. Other effects in COVID-19 include addressing chronic inflammation, which is suspected to produce many of the long-term effects. Vagal nerve stimulation helps with that.

To reiterate, with COVID-19 you have an immune response, and a lot of cytokines are released into the system. In a well-functioning system, you may be able to modulate that down. But the majority of us do not have perfect function in these areas. These areas may not be very viable or well integrated, and their output can be significantly compromised.

Then we see the output of the dorsal motor nucleus of the vagus producing changes related to cholinergic suppression of inflammatory mediators.

With all that said, I think you get the idea of how vagal nerve stimulation works. I think you understand a little bit of the difference between the galvanic stimulators and their neuromodulatory effect, compared with the systemic and neuro-remodeling effects of pulsed radiofrequency.

So now we’ll focus a little bit more on that.

What are the stimulation sites?

There are two main areas because that’s where the vagus nerve can be accessed. You have the auricular areas, including the cymba conchae and the tragus. Then you have the cervical area, usually over the sternocleidomastoid region, around this area.

The question is: which is the best site? Do you do cervical stimulation or auricular stimulation?

Currently, the general thought is that auricular stimulation seems to be the better choice. Why? Because it’s easier to find the stimulation point. Pretty much anybody can find the cymba conchae. You can see it, put a probe on it, and stimulate that area.

The question then becomes: between these auricular areas, which is the best one?

That is difficult to answer because different research studies have used different protocols. Some have used the tragus. Some have used the concha. Some have used the cymba conchae as the primary stimulation point.

My recommendation is that they all have a chance of working. If you find that the cymba conchae is not working for your patient, maybe try the tragus. Be open to the fact that you can go between these different areas.

The idea is that everyone is probably going to be a little bit different.

Let’s look at the stimulators themselves.

There are basically two technologies in these stimulators. One technology is interrupted DC galvanic stimulation. The other technology, used by the Stimpod, is pulsed radiofrequency plus interrupted DC galvanic stimulation.

As far as I know, there are no commercially available transcutaneous pulsed radiofrequency stimulators other than this type of technology. I may be wrong, but I couldn’t find them. If anybody knows of some, please let me know.

What are the contraindications?

Vagal hypersensitivity. If your vagus nerve is already kicking in and you are hypersensitive, it is probably not a good idea to stimulate it.

Other contraindications include haemophilia, psoriasis, pimples or skin lesions over the stimulation site, and active implantable devices such as pacemakers.

Even though you are not stimulating directly over the pacemaker and are stimulating some distance away from it, the idea is that radiofrequency waves are systemic. They travel through the blood to reach other areas. You are also stimulating the vagus nerve, which can impact the output of the sinoatrial node, and so on. You want to be careful, and it may not be worth diving into that side of things.

What are the adverse effects?

First, when you look at the list, it may seem like a lot. But understand these are very rare. We’re talking about around 1% or less on the high end.

The main ones are site discomfort. You might activate Arnold’s nerve cough reflex, where stimulation of the ear causes coughing. That might be augmented.

You may see bradycardia, gag reflex activation, lacrimation, vasovagal syncope, vasovagal reflex augmentation, or some dizziness.

Just be aware that these things can happen when you do vagus nerve stimulation. You may want to warn your patient: “Let me know if you get a little dizzy. Let me know if you get tearing in your eyes. Let me know if you notice any sensory changes.” Not to scare them, but so you know what might be happening.

Let’s talk first about interrupted DC galvanic stimulation.

Its biggest contribution is neuromodulation. That is the functional aspect or functional change.

The main stimulation parameters I could find usually have session times between 8 and 15 minutes.

What I recommend is that, as a clinician, if you want to find out what the actual stimulation time should be, you may want to pick up some biomarkers. Look for changes in heart rate. If the pupil dilates on the side you are stimulating, that is probably not indicative of good parasympathetic output. It may indicate that the system is failing.

Remember, all of these stimulations require energy. The nerve must be able to take in and metabolize the stimulation.

If you are stimulating a nerve and the nerve has neuropathy, damage, or the nuclei in the brainstem are unstable, you may see a failure of activity. You are stimulating, but the nerve basically says, “I’m done.”

An analogy would be asking your 75-year-old grandmother to run a short marathon. She probably won’t be able to do it because she doesn’t have the metabolic capacity.

Be aware of that, and be aware of why pulsed radiofrequency may be a superior way to address it, which I’ll get to in a second.

For intensity, in cardiac applications, most of the studies use 50% to 80% below the threshold that lowers heart rate. I would suggest you incorporate that.

For other conditions, intensity is usually based on patient tolerance.

Frequency is all over the place. There is no real consistency, but from what I’ve been able to find, the 10 Hz range seems to be best at reducing heart rate. There is also one study that used a 30 Hz range and reduced sympathetic activity to muscles.

The Stimpod does 10 Hz, so you should be in good shape for that.

Now let’s talk about transcutaneous pulsed radiofrequency, which is why we are all here.

With the Stimpod, it combines both approaches. You get the benefits of galvanic stimulation, and you also get the very interesting benefits of pulsed radiofrequency.

Here are the benefits you get with this, but not with galvanic stimulation alone.

You get neural remodeling. You get structural changes in axons. You can get more axons and more myelination. You also get systemic effects, not just effects over the area that you stimulate, but throughout the entire body as these RF waves travel through the blood.

You might be treating someone for a headache, and they may come back and say, “You know what, my low back pain is feeling better now,” or “I’m not having as many gut issues as I used to.” Those are the types of things you should look out for.

Here’s another important point. I’ve been talking about energy. When you stimulate a nerve, the nerve needs to metabolize that stimulus. Sick nerves don’t metabolize very well. The problem with a lot of stimulation is that if you don’t have metabolic support, you can get into trouble.

What is beautiful about pulsed radiofrequency types of stimulation is that they energize nerves and other tissues. For nerves, this occurs primarily through a very interesting mechanism.

When you use pulsed radiofrequency, it activates M2 macrophages to donate their mitochondria. They literally donate mitochondria to neurons. That means the neurons can have the energy capacity they need to produce what they need to produce. You need to produce protein, myelin, and many other things, and all of that takes energy.

I think that is one of the most distinguishing parts of the use of pulsed radiofrequency, and it is something that other types of nerve stimulators just can’t touch.

Obviously, this promotes neural remodeling. It promotes neuroimmunomodulation. Pulsed radiofrequency also promotes bone and cartilage growth, and it promotes wound healing in diabetic neuropathy.

In diabetic neuropathy, one of the things to understand is that it’s a metabolic disorder. You have a sugar issue. If it’s a metabolic disorder and you’re trying to stimulate the nerve, but the nerve can’t metabolize the stimulation, you’re in a conundrum.

That is why a lot of treatments done for diabetic neuropathy patients don’t do so well. I’m not saying they don’t work at all, but you could really improve your outcomes by incorporating pulsed radiofrequency into your regime.

I’m giving you the why of how it works so that it makes more sense and maybe encourages you to incorporate this technology.

What are the take-home points?

Transcutaneous vagal nerve stimulation using the Stimpod gives you DC galvanic stimulation, which induces neuromodulatory effects, and pulsed radiofrequency, which induces systemic and neural remodeling effects.

Ultimately, no direct comparison currently exists between auricular VNS and cervical VNS. As I mentioned, there are some reports suggesting that auricular vagal nerve stimulation may be preferred simply because most people can’t get the location wrong. It’s a little harder to find the vagus nerve in the neck.

You also have other structures in the neck, including muscles. When you use galvanic stimulation, you can create a muscle contraction. Whenever you create a muscle contraction, you activate the sympathetic system.

The biggest challenge in the literature right now is figuring this out: what are the ideal treatment times, intensities, frequencies, and pulse widths for the galvanic portion? A lot of the research is based on galvanic stimulation.

My opinion, based on the complementary mechanisms of both DC galvanic stimulation and pulsed radiofrequency, is that combining the two just makes sense. To me, it’s a no-brainer. I think that is what we’re seeing from the feedback from the community of clinicians using Stimpods and this technology. They are seeing some remarkable results.

One last thing before I finish: another big question is where to place the grounding electrode when doing vagal nerve stimulation, especially using the Stimpod.

You have the probe. Where do you put the grounding electrode?

The idea with the grounding electrode is that you don’t want it too close to the point of stimulation. There are some suggestions that placing it over the stellate ganglion may be beneficial because the tissue underneath the grounding electrode, especially if it is neural tissue, may be inhibited.

You may not want to put it over the carotid bodies because you don’t want to inhibit them. So you may put it over the stellate ganglion or on the trapezius.

The next question is whether you put it on the same side or the opposite side.

Interestingly, in the studies I mentioned regarding intravenous pulsed radiofrequency, they placed the grounding pad on the contralateral side of the body. I think what they were trying to do was get the pulsed radiofrequency waves to spread throughout the entire body and go to the opposite side.

They did talk about that in the articles, but more from a “this is what we think” standpoint. So the opposite side can work, as can the same side. At least for vagal nerve stimulation, I would probably focus on the stellate ganglion.

All right. Thank you, everyone. I hope you found the information in today’s webinar valuable, and I hope it has maybe opened your eyes to incorporating vagal nerve stimulation into your office.

For those of you who are already incorporating vagal nerve stimulation, I would encourage you to seriously consider using a device that also incorporates pulsed radiofrequency. What it does and how it does it is seriously amazing.

I’ve been at this for a lot of years, and I do a lot of reading, as Dr. Garcia will tell you. Just for this presentation, I went through about 40 articles to gather and summarize this information for you.

There is a lot of good information out there, a lot of good progress, and a lot more research happening. Thank you.

Dr. Freddys Garcia:
Excellent job, Dr. Klotzek. I love that presentation. You can see that you took a lot of time to go through it.

I know some people may want references, so you can see Dr. Klotzek’s email address up there. If you have questions or want some of the references, email him and he’ll share them with you.

That was wonderful. There was one question somebody asked: do you think vagal nerve stimulation can help with multiple sclerosis, MS? What do you think? I have some thoughts.

Dr. Adam Klotzek:
Absolutely.

One of the consequences of MS is inflammation and neuroimmune dysregulation. Anything you can do to help reduce inflammation and promote better neuroimmune balance is sure to help.

If you look at it from a pain standpoint, you can use vagal nerve stimulation to activate those descending cholinergic fibers that come from your brainstem. That can help on the pain side.

On the nerve regeneration side, with MS, myelin is being attacked. So you need to support myelin production. As I mentioned before, when nerves are sick, they are not as metabolically capable.

If you are using pulsed radiofrequency, it can help energize those nerves so they have the metabolic capacity to produce the myelin that the immune system is attacking. So yes, it could be very beneficial.

Dr. Freddys Garcia:
That is exactly my sentiment as well.

Awesome. Great question.

To everybody watching the seminar, sorry that we went a little bit over time, but Dr. Klotzek has a lot to share. Thank you very much for your time today, Dr. Klotzek. It was amazing.