All right. Good evening, everyone. Thank you so much for joining us today with an excellent webinar. With the pleasure to have the legends and the experts of the field of neuromodulation in craniofacial pain today. This webinar is ran by educational committee of North American neuromodulation society. And we had the honor to have pioneers of this field and also the people who have the most expertise and knowledge in craniofacial pain. I'm going to start by introducing our panelists and we'll get to the discussion. And I'm confident that this is going to be a very educational and eye-opening for our audience. So we have great panelists, starting with Dr. Konstantin Slavin. Dr. Slavin is a neurosurgeon and he is the professor and head of section of sirtactic and functional neurosurgery at University of Illinois. And our second speaker is Dr. Samer Nourrooz. He's the professor of anesthesiology and pain medicine. He's the chairman of center of pain medicine at Western Reserve Hospital in Ohio. He's a founder of American Interventional Headache Society and previous president of American Society of Regional Anesthesia and Pain Medicine. And we also have today Dr. Miles Day. He's one of the, I would say the best experts in neuromodulation and headache. He's the program director of the pain fellowship in Texas. And also he is one of the best teachers that I've ever seen for craniofacial pain and neuromodulation. And today is his 200th anniversary of lectures, worldwide education of neuromodulation in craniofacial pain. So it's a pleasure to celebrate that with Dr. Day. So to start with, we will have like a different topic. So the first topic is going to start with Dr. Slavin on indications and mechanism of neuromodulation for craniofacial pain. And we will follow with Dr. Nourrooz lecture on patient selection in craniofacial pain, followed by Dr. Miles. They talk in about treatment types and variations. And I will add some slides at the end and brief talk on emerging technologies for craniofacial pain. Dr. Kiran Patel had a conflicting in schedule. So she was not able to join the webinar today. And Dr. Slavin has been traveling. So, but kindly he was able to record his lecture, but he is so dedicated that he actually joined the webinar himself right now too. But because he might be at the airport, we're going to start recording unless he feels confident that he will be able to give his lecture with minimal noise, but I think he's walking at the airport. So we were going to go with the recorded video. Good afternoon, everybody. First of all, let me apologize for not being able to join you in person. It just so happens that I'm traveling right now on my way to the conference in Dubai, and I didn't want to be interrupted by the airport noises while we're having this wonderful webinar. Second, I would like to thank all the hosts and moderators and particularly Dr. Shraghi, who put a lion's share of work into putting this together. The webinars is a difficult job, and he did an amazing job of putting together the program, the speakers, the arrangements, and so forth. So without further ado, let me start with my presentation. And I would like to start by saying that a lot of topics presented today will probably be overlapping each other. And I apologize in advance if I am saying something that my colleagues are planning to say during their talks. So anyway, let's just go with the slides. And the topic that I'm talking about has to do with indications and mechanisms of neuromodulation in treatment of craniofacial pain. The disclosures, I believe, have already been shared by the organizers. And I will proceed with the rest of my talk. So to begin, my name is Konstantin Slavin. I'm a professor in Chicago, University of Illinois, and I just happen to be the president-elect of International Neuromodulation Society. But in the past, I worked with Nance and was secretary of Nance, and that was a great time. And I am remarkably happy to see how well Nance is doing these days. Now, in addition to disclosure about my conflict of interest, which used to be quite few, and now less and less because of the requirements of the INS work. However, there's some other disclosure I have to mention, because I am very biased towards neuromodulation, and a lot of my publications have to do with that. One of the books that came over the years was actually on neuromodulation for facial pain. So that does not make me expert in this by any means, but at least it tells you that I read all the articles and are familiar with literature. Anyway, neuromodulation for craniofacial pain has been around for a long time. Now, we talk about 1965 as a time of birth of gait control theory of pain, and 1967 when the first spinal cord stimulation device was put in. But it turns out that neuromodulation was used for facial pain even before that, when in 1962, our colleagues, neurosurgeons from California, implanted the patient with neuropathic pain with neuromodulation device that was delivering stimulation at 14,000 hertz. Since that time, people tried a variety of other targets and not just the nerve itself. And as you can see from this publication that came out seven years ago, people stimulate pretty much everything. This particular patient documented here has a stimulator over his cortex, the deep brain stimulation device, the device in the foramen ovale, in the sphenopelatine ganglion, in the vicinity of gasserian ganglion, the supraorbital stimulators put in. And if you think that's the only patient who has this type of complex, now the same paper has a second example, which once again has a patient who has been implanted with many devices at once. Motor cortex, deep brain stimulation, gasserian ganglion, sphenopelatine ganglion. And these are just a few examples of what can be stimulated. Now, the fact that there are patients who have all of these devices at once tells you one thing, that nothing really works in a guaranteed fashion, and there's always room for improvement. Now, there'll be more talks about it later today, but I will just talk about the general principles of neuromodulation, the indications, and perhaps some mechanisms of action. It's important to understand that there are more than one classification of these conditions, and the most common neurosurgical classification was created by Birchfield exactly 20 years ago. At that time, he stratified all trigeminal pain into several categories. And as you can see here, very few of these can be treated with neuromodulation. However, the majority of neuromodulation practitioners are not neurosurgeons, and therefore, they primarily use the system which is designed by pain specialists. And the classification of facial pain that came out 10 years ago is a little bit more comprehensive. We analyzed all of these classifications and came to the conclusion that this one, which is ICHD3 beta classification, is probably one of the best examples of comprehensive facial pain and headache. The underlying conditions here are the ones for which neuromodulation is clearly indicated and is being used today, and those include painful near-trigeminal neuropathy, post-therapeutic trigeminal neuropathy, post-traumatic trigeminal neuropathy, the occipital neurology of the central post-stroke pain, and perhaps persistent idiopathic facial pain, which I know is the subject of many investigations these days. Everything else, including classical trigeminal neurology, glossopharyngeal neurology, geniculate neurology, pain from optic neuritis, the ophthalmoplegic neuropathy, those are not good indications for neuromodulation for variety of reasons, and we can talk about it separately at a different webinar if it ever comes to that. However, what's being used for this can be classified by the target, and the targets are many, because trigeminal pathway is a well-established pathway, and there are definite structures that can be responding to neuromodulation in a predictable way. Now, some of them are central structures that are located intracranially, and we're talking about more cortex stimulation or deep brain stimulation. There are some central structures in the spinal canal, like spinal cord stimulation, but you can also stimulate the actual trigeminal system, trigeminal root, trigeminal ganglia, and trigeminal branches. You can stimulate the area outside the trigeminal nerve, which is occipital neurostimulation, a great example for craniofacial stimulation, and you can stimulate autonomic structures, and spinal palatine ganglion is a perfect example of autonomic structure that can be stimulated in order to control certain types of facial pain. What we're going to talk about today is primarily about mechanism of action for these modalities, and then my colleagues will discuss each of these things in their own place within the algorithm. The mechanism of action for peripheral structure seems to be somewhat similar, so I don't know any differences between stimulation of trigeminal branches or any other peripheral nerves, because even though it is a cranial nerve, the general structure is very much the same as it is anywhere else in the human body, and that's where we normally use gait control theory of pain. Now, this theory was postulated in 1965. It was illustrated by peripheral nerve stimulation in 1967, and ever since that time, we've been using it, even being aware of all of its limitations and shortcomings. It still works quite well explaining the action of the paresthesia-inducing stimulation, because whenever paresthesia is turned on, the pain tends to subside. This concept of a gait control mechanism that allows you passage of only one type of information definitely makes sense when we talk about paresthesia-inducing modalities. Paul and Sweet, who back in 1967 tried to illustrate and experimentally confirm the gait control theory of pain, actually stimulated themselves on the intraorbital nerve location, which is exactly what we're talking about right now. So, this theory applicable to craniofacial pain control has been well supported by the literature for the last 60 years. What about the other aspects of it? Now, the stimulation of the trigeminal system tends to elicit central responses beyond the gait control mechanism. There is a change in the central excitability of both dural afferents and within the trigeminal cervical complex, and that explains why even occipital nerve stimulation may control facial pain and may control the headaches. The central mechanisms at the level of the trigeminal nucleus definitely explain why pain can be suppressed by the stimulation even outside the trigeminal area. If you think about this, the mechanisms of the peripheral stimulation are quite complex. There are many synapses that travel from the trigeminal nucleus throughout the brain, including the intrinsic pain inhibitory pathways within periaqueductal gray or periventricular gray. There's a lot of connection through both medial and lateral sensory systems that have to do both with somatic perception of pain and this emotional component of that. And the chapter that Dr. Barsh and Dr. Goldsby published in one of our books more than 10 years ago is a very great thing to read in order to understand all of these concepts. The spinal cord stimulation is used for the control of facial pain, and the question arises, why spinal cord stimulation? What does spine have to do with face? Now it turns out quite a bit. The first person who discovered this was Dr. Barolat, past president of Neuromodulation Society. When he found that stimulation at the high cervical level with an inferiorly directed electrode could generate paresthesis in the lower part of the face, he was not surprised to do this. He's a neurosurgeon, so he knows that there is a target for trigeminal interventions in the spinal cord, and that's where the trigeminal nucleus is located at the level of C1 or C2. And those pathways, interestingly enough, do not follow the branch distribution. So they don't go by one, two, and three like you would normally see in the rest of the trigeminal system. They go by this onion skin distribution with most central area around the mouth being located above the obliques of the fourth ventricle, and more lateral aspect descending down to C1 or even C2. Now this has been going on for a long time, and therefore, when we use neuromodulation, we are very capable to cover the lateral part of the face, and it's very hard to cover the perioral or central part of the trigeminal thing. Now one of the things that we use quite often for really complex and complicated neurobiotic conditions is what's called motor cortex stimulation. Now motor cortex really does not participate in sensory perception. So why would you stimulate motor cortex to control somebody's pain? Now that was discovered serendipitously when people tried to stimulate sensory cortex, and they noticed worsening of pain as a result of the stimulation. However, when they stimulated adjacent motor pathways, the pain has subsided. And now there's multiple explanations for that. One of them has to do with downstream inhibition. So when you stimulate motor cortex, you're actually stimulating the structures in the brain through these non-specific pathways. So this was postulated back in the 90s when motor cortex stimulation was described as a modality, and there were some illustrations for that, because when you stimulate motor cortex and sensory cortex and record from the thalamus, you can see immediate inhibition of activity when motor cortex is stimulated. This downstream inhibition has also been documented when our Brazilian colleagues investigated this by stimulating ipsilateral and contralateral motor cortex. They discovered that ipsilateral motor cortex poses significant suppression of the signaling and contralateral does not. So this is something that kind of explains why the motor cortex stimulation works on contralateral part of the body, because the ipsilateral thalamus gets inhibited by the motor cortex. Now there's also a concept of with a cortical basal ganglia cortical loop. Sometimes cortical basal ganglia thalamic cortical loop. This is well established for the treatment of motor disorders, but the same mechanism can be used for explanation of control of pain. So this is something that we definitely employ, and when we stimulate motor cortex, we see effects almost immediately. The motor cortex stimulation also activates the cingulate cortex, which is a part of the limbic system and is involved in the processing of pain. So by stimulating the neuropathic pain patients, we know that cingulate cortex actually does get activated, and the PET scan convincingly shows that. This is not the only example of that. If you look at more illustrations from the same paper, you can see that activation is quite robust, and it tends to correlate with the energy and power delivered to motor cortex. So there's direct connection to cingulate when motor cortex gets activated, and these changes can obviously explain some of the pain-related mechanisms. There's also descending activation. Now we talked about descending inhibition, but it turns out the descending activation goes all the way to the parietal brain. So we can actually stimulate pain-inhibiting structures, and by doing that we can control the pain in a more diffused fashion. The descending activation has been also investigated by our colleagues from Brazil, and they discovered that there's a significant increase in the firing of the neurons within the pain-inhibitory system of the periaqueductal gray neurons. So this is something that probably has to do with non-specific motor cortex stimulation effects, when there's not somatotopic reorganization, but more like the general inhibition of the pain. Now it's somewhat different when it comes to the autonomic nervous system, because the autonomic nervous system has its own pathways in both pain production and pain suppression. In the intranuclear region, the sphenopelidenganglion is a structure that we stimulate. It was shown quite a long time ago that if you stimulate sphenopelidenganglion at a lower frequency, you can elicit the pain, particularly cluster attacks in cluster attack patients. But stimulating at a higher frequency, you can control the pain. And how does this happen? I mean, there's a nice animation kind of showing you this, that when the signals travel from the autonomic system to the meninges and then back into the trigeminal system, the stimulation of sphenopelidenganglion can break this vicious cycle, can interrupt the circuit, and therefore control the pain. Now what we tried now is to start to synthesize all this and have all these different mechanisms when we choose appropriate modality for appropriate patient, because every patient's pain is different. And if it has autonomic features, it probably will have a higher chance of responding to autonomic stimulation. When it has features of decrementation, then peripheral procedures do not work and you have to choose more central things. If the patient has a stroke and the facial pain is a result of the stroke, then even spinal cord stimulation is unlikely to help. And you have to go to either deep brain stimulation or mortal cortex stimulation. However, if you do have peripheral problems, such as in neuropathic pain, after trauma, or even after a herpetic infection, then stimulating at the level of spinal cord or stimulating at the level of periphery throughout the trigeminal system is definitely something worth considering. So I hope that this brief summary serves as a good introduction for the topic and I look forward to hear my colleagues speak about it. I personally will stay live during this webinar and I will try to participate in questions and answers. But thanks to this recording, I hopefully was able to avoid all the airport sounds that will distract you from my presentation. Thank you very much for your attention. And as I end this, I want to bring your attention to two conferences that will happen over the next few months. One will be in Chicago, in the place where I am right now. In the beginning of September, we'll have the World Congress of Stereotactic and Functional Neurosurgery. But the highlight of the year will be the INS Congress that will be in May of next year in Vancouver, British Columbia, Canada. So you will be invited and I look forward to see you all there. Thank you very much for your attention. Wonderful. Thank you so much, Dr. Slavin. Great lecture, as always. So without further ado, we will follow with the second presentation by Dr. Samer Noorooz, neuromodulation for chronic pain, craniofacial pain, regarding the patient selection for this patient population. The podium is yours, Dr. Noorooz. Thank you very much. Thanks for having me here with this wonderful panel. When it comes to patient selection for neuromodulation of craniofacial disorders, I would like to first make sure we are talking the same language. So I'm going to go briefly over terminology, because this is very important. Diagnosis, differential diagnosis, patient selection, and then the role of trial and the role of peripheral nerve blocks prior to trial and implant. So terminology is very important because still, unfortunately, most of the surgeons that are using this trigeminal neuralgia or type 1 and type 2, which is really obsolete now, and on the other hand, most of pain physicians still using atypical facial pain, which is again, does not exist anymore. So to be clear, these are the three major craniofacial pain disorders that, as an interventionist, we get referral about them. And we need to distinguish them very, very clearly, because the response to pharmacological management are different, and not all of them, like Dr. Slavin stated, respond well to neuromodulation. So trigeminal neuralgia, this is the typical trigeminal neuralgia that we're aware of. Classical trigeminal neuralgia, if they have neurovascular compromise. Basic trigeminal neuralgia, if they do not have neurovascular compromise. Secondary trigeminal neuralgia, if it's typical trigeminal neuralgia, no neurovascular compromise, but there are other causes that known to cause trigeminal neuralgia, mainly MS and tumors or space-occupying lesions. Then trigeminal neuropathy, usually this is trigeminal neuropathy associated with shingles or post-herpetic trigeminal neuralgia, post-traumatic trigeminal neuralgia, or if there is no known reason, we call it idiopathic painful trigeminal neuropathy. So post-herpetic neuropathy, post-traumatic neuropathy, and idiopathic painful trigeminal neuropathy. And then this should be included in the French diagnosis, which is TACS, or trigeminal autonomic syphilanges, cluster headache, sanctum, or hemicranial continuum. So history of physical exam is very important. The side lock, if it's unilateral or bilateral, this is a huge difference in the working diagnosis for headache disorders and orificial pain, which distribution, which nerve. Neurologic features or not, neurological deficits or not, any involvement in the eye, ear, TMJ, teeth, mouth, history of trauma, rash, accidents, and definitely neurological symptoms or signs. Any patient who is complaining of persistent facial pain should get a dedicated imaging, best MRI, with special protocol for trigeminal neuralgia to rule out neurovascular compromise. So this is a typical facial pain case, 65 years old, she has a few months history of right face pain, many attacks a day, it's unilateral, the last few weeks, few seconds. No history of trauma or rash, no neurological deficit, and eye movements are okay. So those in the red are the most important questions that we're missing from this case. What is the pain? Temporal, you want to make sure it's not temporal arthritis, joint cell arthritis, which branch, orbital, cavernous sinus issues, autonomic features, rule out cluster headaches and sanctum and hemicranial continuum, what's the triggers, which are usually the trigger zone for trigeminal neuralgia. So this is the International Classification for Disorder Diagnostic Criteria for Trigeminal Neuralgia. Usually, it's unilateral. Very rarely, it's bilateral. Actually, if you have bilateral trigeminal nerve pain, you should think about MS until proved otherwise. It's electric shocks, lancinating, seconds. So what's trigeminal neuralgia? We said it's classic, which is the middle. You do MRI. It showed neurovascular compression, not just contacting, not just touching, and you have to compare it to the other asymptomatic site because if they are the same, then there's no need for neurovascular decompression or surgical options. So it has to be clear compression or compromise. This is what type 1 and 2 used to say is pragmizimal, it's type 1. You have a background of pain, it's type 2. Actually now, classic trigeminal neuralgia can be purely pragmizimal or can be constant pain. Adiabatic if there is no reason. Secondly, if there is another reason to cause trigeminal neuralgia, which is usually tumors or MS. Why I put here, the differential diagnosis is a big list. There is lots of options, went through it briefly in the previous talk, but I put here the Sankt and the trigeminal autonomic syphilalgia because they can really be confusing as trigeminal neuralgia. Usual trigeminal neuralgia, V2 and V3, V1 alone is very rare. V1, trigeminal nerve pain, you want to make sure it's not shingles. Usually the patient has history of rash. On the other hand, TACS or trigeminal autonomic syphilalgia, it's V1 more. All severe. The duration is really, really short with Sankt or SUNA. Autonomic feature is the main differentiation. Autonomic feature, drooping of the eye, lacrimation, stuffy nose, all this more with trigeminal autonomic syphilalgia. Spontaneous attacks only, it's more in the trigeminal autonomic syphilalgia. The treatment is totally different. Similarly, trigeminal autonomic syphilalgia can respond to endometasin or prevention lamotrigine. The oxycarbamazepine or carbamazepine, this is more for trigeminal neuralgia. Also the intervention is totally different. The target, the neural, the network that's responsible for trigeminal neuralgia will be the trigeminal gazillion ganglion with the trigeminal autonomic syphilalgia will be the sphenopelatine ganglion. So it's totally different targets, how we reach out to here by doing a great history, exam and imaging. This is a nice algorithm, clinical algorithm to come up with appropriate diagnosis. So if there's history of trauma, you want to do imaging to make sure there is no fissure fracture or any cystic leak or something. Elderly patient, female patient, you want to rule out temporal arthritis or giant cell arthritis. Neurological deficit, you have to get an imaging of the brain. Then rule out other factors like NETI, TMJ causes. Autonomic feature, you consider headache disorders, mainly trigeminal autonomic syphilalgia, subset of patient with migraine and self-cogenic headaches, as well as occipital neuralgia and have autonomic features as well. If there is no reason, it's persistent facial pain. This is what we used to call atypical facial pain. Now it's persistent idiopathic facial pain. There's lots of psychosocial, sociosomatic issues that need to be addressed before considering invasive therapy. Definitely neuromodulation for craniofacial pain is not a mainstream therapy. It's only for those intractable patients that they have an appropriate diagnosis and failed conservative treatment. Patient selection, I like this statement. It's much more important to know what sort of a patient has a disease than what sort of the disease the patient has. Because pain is an experience, painful stimuli, and there are reactions or the pain experience that's dependent on multiple variables. It could be societal factors, biological factors that you don't have much to change, although you can always counseling about smoking, weight loss, opioid use, and then the psychological determinants. That's why we usually require psychological evaluation to make sure that any other psychological disorders are addressed appropriately. So there is not much literature about the role of the trial in regards to peripheral nerve stimulation or cranial nerve stimulation. So we can extrapolate the information that we are more familiar with in regard to spinal cord stimulation. Earlier this year, this was a consensus guideline published on behalf of Azra Pain Medicine, Nance, the IRN, the Azra, and the Canadian Neuromodulation Society. So for patient screening, we should not include patient with active psychosis or untreated substance use disorder. We should screen all patients for depression. However, depression alone is not contraindication, because depression can be a reaction from suffering chronic intractable pain, untreated pain. So we need to refer to the specialist to make sure it's well-controlled and it's not major depressive disorder. The other issue is during the trial, it's okay for the patient to continue interventions, pharmacological non-interventions, non-pharmacological options as needed, because patient might be on opioid for other reasons, knee arthritis or back pain, and you are monitoring the success of your cranial nerve trial based on opioid consumption while the patient still need them for other painful options, diseases. Nowadays we have information in the field of spinal cord stimulation that worse outcome was smoking, high pre-op opioid use, as well as high BMI. So it might be a good opportunity to counsel the patient about the potential for low or less than optimum outcome. So what's the expectation? I think this is the most important factor in discussing this treatment option with the patient. Expectation from a trial is different than expectation from the permanent plan. So I'd like to separate the discussion, two different occasions. Expectations could not just pain. Unfortunately with the CMS-LECD, they require 50% success, but it's a global experience. Every patient is a different story. So some patient maybe if you drop 20, 30%, they can function better, all what they need is to have a better golf game or walk the dog. This is important. So we should have individualized patient expectations. This is the letter that the FDA sends to all pain physician and neurosurgeon, whoever is implanting. It was issued in the end of December, 2020. We received it in January, 2021. It's a reminding that we have to do a trial prior to spinal cord stimulation. And successful trial means 50% pain reduction. Again, this is in case of spinal cord stimulation, but most of the clinicians apply the same to peripheral nerve stimulation. So what's the terminology of why we need trial? If you're using prosthesia-based because you want to make sure that you are covering the painful areas, patient like the sensation, it's tolerable. And then you measure the outcome, whatever the outcome that you agreed with the patient was. Usually it's pain, but more important function, sleep, plus or minus medication change. I think the most important one is not just the pain relief. I think it's the overall satisfaction and the function improvement. Analgesic use can be confusing because most of the patients, they are medication for other things. Facial pain, usually we don't prescribe opioids for facial pain in general. They are on opioids for other painful issues, back issues, osteoarthritis issues. And counting on decrease in opioid dose for those patients is unfair. So I like the SMART, which is specific, measurable, achievable, realistic, timely, and last long term. So extrapolated recommendation that we can apply to peripheral nerve stimulation, all patients should be evaluated for efficacy and tolerability of the trial. We should be able to cover 80% of the painful area, relieve at least 50%. If less than 50%, then you need to document function improvement, reduction of medication, sleep improvement. This was published literally online a couple of days ago, and yesterday I had to add this slide. This was published in Neuromodulation, the role of diagnostic nerve block in peripheral nerve stimulation. It's a 10-year experience in one institution, which was the group from Mayo Clinic. They found that diagnostic block was not associated with superior pain relief at three or six months after peripheral nerve stimulation implant. Only diagnostic block may potentially predict the short-term pain relief from the temporary lead, but not associated with better outcome at three or six months. And we saw this in the case of occipital nerve stimulation, that the patient that had positive response to occipital nerve block were included only in the study, and then there was another arm that we added, the patient that had negative response to occipital nerve block, and then still we went ahead and implanted them, the results in both groups were the same. You need diagnostic nerve block, I think this is an important point to distinguish. You need diagnostic nerve block to make a diagnosis of the disease. Like occipital neuralgia, you cannot make a diagnosis of occipital neuralgia unless almost complete pain or pollution on occipital nerve block. And by the IHS means more than 90% relief of pain. This is a diagnostic nerve block to make the diagnosis. And the same with most of the other cranial neuralgia, you need a diagnostic nerve block to make a diagnosis, and clinically this is what we see, it does not really predict good outcome. The trial, I think, is much more valuable. So moving forward, I think we need focused research about the importance or the need for diagnostic blocks or trial prior to preferred nerve stimulation. We need research for the reason, for a good reason, for the right reason, with the patient and the center of the research, not just to add another diagnosis to get it approved. What are the patients that can have a better outcome? What are the variables? What are the outcomes that's meaningful to the patients? Again, back to the SMART outcomes. So I'll stop here, and I think by the end of this session we'll be available to address your questions. Thank you very much. Thank you, Dr. Nourouz, a wonderful presentation. So the next topic we will present today will be by Dr. Day on types and variations of neuromodulation for craniofacial pain. Dr. Day, please. Perfect, thank you. Share my screen with everyone. I wanna thank everybody. Those were great presentations by Konstantin and Samer to look at how things work and how we choose patients. Cause I think that's a very, very important patient selection I think will improve your success. Another thing as a reminder is that the neuromodulation we're talking about is not the first thing on your algorithm of treatment. You must follow an appropriate algorithm going from your conservative therapies with medications and then your minimally invasive procedures. And all those have to either fail or not provide adequate pain relief before you consider neuromodulation in your treatment algorithm. The different types of neuromodulation we target is either central or peripheral. And Dr. Slavin gave a good presentation on deep brain stimulation and motor cortex stimulation. As far as myself, as far as an interventional pain management specialist, my tools come in when we look at caesarean ganglion stimulation, nucleus caudalis stimulation centrally. There's also some non-invasive procedures that can be done with transcranial direct current stimulation, the CNS, and also transcranial magnetic stimulation. And peripherally, we look at peripheral nerve stimulation and peripheral nerve field stimulation. And honestly, I think when we look at the peripheral procedures, it's more peripheral nerve field stimulation as opposed to peripheral nerve stimulation. Because with peripheral nerve stimulation, we're really talking about placing electrodes directly on the nerves. And when it comes to using neuromodulation for facial pain peripherally, if the leads are actually sitting on the nerves and they're in muscle, the stimulation is going to cause muscle contraction, which is very painful. So in my opinion, it's really peripheral nerve field because we're subcutaneously stimulating a field. There's a book that our colleague, Dr. El-Sayed, had put together on trigeminal nerve pain. And this is an algorithm of treatment that's in the chapter that we wrote. When you look at the neuromodulation algorithm, I corrected it somewhat because this algorithm said neuromodulation for trigeminal neuralgia, but it's really trigeminal neuropathic pain is what we're targeting, not necessarily trigeminal neuralgia. Although there are some instances where I have used neuromodulation for trigeminal neuralgia when the other procedures were ineffective. So briefly about central stimulation, Dr. Slavin did a great job talking about deep brain. I am not a neurosurgeon. I did not sleep at a Holiday Inn Express last night, so I'm going to stay in my lane. For questions on this type of deep brain and motor cortex, I will point you towards Dr. Slavin, but deep brain has been done since the early seventies. There are different targets when we're looking at neuropathic pain and nociceptive pain. This is a very invasive procedure because it requires a craniotomy. And this is just some slides, not from my patient, but from an article in neuromodulation in 2014. So it's definitely a much more invasive procedure. Motor cortex stimulation, as Dr. Slavin was saying, first reported many years ago. Meyerson reported in 93 to treat facial neuropathic pain. And as Dr. Slavin did an eloquent job of going over how stimulating the motor cortex actually helps the pain through the sensory system. So I've learned quite a bit from that. I think it's always important that as educators, we learn from our colleagues, but the experts, and we learn from our students, and we always should continue to learn. This is just an example. These motor cortex stimulation are actually, they're paddles that are placed over the motor cortex, not necessarily in the motor cortex. And sometimes this is done with a patient who is sedated and then woken so that they can make sure the stimulation is in the correct area. Now, gasserine ganglion stimulation is also central stimulation because you're actually using, one thing that should be mentioned is that all the use of these leads are off-label use of currently available SCS leads. This was an article that I just found today by Gupta et al in 2020, showing gasserine ganglion stimulation, the placement of electrode through foramen of valley, and how each of these contacts on an eight contact lead with very narrow spacing is used to stimulate the different parts of the gasserine ganglion because of the three divisions, ophthalmic, maxillary, and mandibular. And one thing that Gupta looked at in his patients were the parameters that they used when they stimulated gasserine ganglion stimulation. So they were using frequencies of a thousand Hertz, pulse widths of 60 to 220 milliseconds, and an amplitude of a half to three volts. So these are the parameters they used. When you look in the literature, there's various parameters, but in their patient population, these were the parameters that were most successful in treating their patients. Now, one thing to remember in order to put this 1.3 millimeter lead into the gasserine ganglion, you have to use a 14 gauge needle, and yes, it does bleed. So if you're gonna do this, you just keep that in mind that you will get some bleeding. This is an example of a 14 gauge, your standard SCS introducer lead going through foramen of valley and an eight contact lead. Looks like three contact leads with two millimeter spacing. This is a slide, the CND that I use from a colleague of mine showing a combination of gasserine ganglion stimulation and also our peripheral lead that you can see out here. So this one is foramen of valley stimulating mostly V3, and then there's a peripheral lead. So sometimes you have to use combinations of techniques when it comes to the leads in order to get adequate coverage of your patient's pain. This is a patient of mine. This is a, once again, a 14 gauge needle. This is not your standard close compact leads, but this patient mostly had V3 pain. And I had performed a trigeminal ganglion RF that helped part of the pain, but she still had tongue pain. This is a patient who had a microvascular decompression that helped for several years and the pain came back. And the surgeon went back into look to re-explore, didn't find any compression of the trigeminal tract and decided to do a conventional RF and a general anesthetic. And the patient woke up with horrible lancinating tongue pain. And so as you can see, sometimes the treatments we utilize to help treat pain can cause pain just like the trigeminal RFTC can result in deafferentation pain. So nucleus caudalis stimulation, another form of central stimulation, your target is C1-2. You're looking at the nucleus caudalis because of the nociceptive afferents from the trigeminal nerve in the C2 region can modulate pain in the occipital region and in the trigeminal distributions. So this, there's two ways to do this. This is one of the ways we had done it way in the past using an off-label use of a paddle lead going over the arch of C1, pointing downwards towards C2. The one thing about these leads is that they were never developed to assume this sort of angle. So these tended to cause some fractures. If they weren't braided leads, you would get a fracture right here on the wiring and then this lead would stop working. So we had done this in the past since probably the early 2000s with the help of our colleagues from neurosurgery. And it did provide some benefit until we had lead fractures. And then of course this causes scarring. And so there's the concern that taking it out would possibly cause dural tears. So we somewhat had abandoned this in the past. Then we looked at using percutaneous leads entering at C7T1, T1-2 and advancing them. As you can see here, up to target C1-2 or as high as these leads can go for the mucous caudal stimulation, you can see this lead. This is courtesy of Dr. Adnan Al-Kaizi. And one of the things that we always had issues with is that when we were placing these leads, the patients were prone on the table and you could advance the leads as high as you can go and you would get great stimulation of the face, usually V2, V3, V1 was very difficult. As Dr. Nehruz was saying, if you have a patient with V1 pain, you should really think about post-therapeutic neuralgia as opposed to a trigeminal neuralgia because that's typically the cause. Even if they haven't had lesions, there's the concept of Sine Herpete or shingles without lesions. But the question is how do you program these things is talked with Dr. Al-Kaizi, you can see the programming here on the left. But the one thing I did find with these is during the trial, you would get good stimulation on the table, you would anchor this to the skin, the patient would sit up, the lead would drop a space or two and then all you would get was next stimulation. So on some occasions we had actually, when we're using SCS, the Nucleus Condylus, we would actually cut down and anchor the lead like we were doing a permanent to fascist so that hopefully when the patient assumed an upright position, that the lead didn't drop. Just another example with Corey Hunter in pain physician 2019, showing images of high cervical stimulation. This was more up around C1-2, as you can see here, as opposed to a little bit higher, which would be the preferable position to account for any movement of the needle with gravity. Complications of central, these appear of course, are with more of the invasive types, infection lead revision with fracture lead erosion, I guess, lead fractured in here, and then some minor complications with more of the central techniques, such as DBS and motor cortex. Now, peripheral stimulation, we're targeting the trigeminal nerve, it's peripheral. When you look at the different branches, you can target superorbital, supratrochlear for neurologists and migraines. Typically for migraines, it's also associated with placing an occipital leads, kind of two superorbitals and two occipitals for the migraines. Infraorbital for neurologists, and we've also done auricular temporal for intractable headaches. Now, these are subcutaneous stimulation. Like I was saying earlier, this is peripheral nerve, this is peripheral field, but really it's more peripheral field because you're trying to stimulate an area. And typically if it's more of the V2, V3, you may end up putting in two leads as opposed to one, if it's purely like a superorbital neuralgia. Implantation is important. You got to look at the qualifications and there's probably a limited number of interventional pain management physicians who will place leads in the face. If a physician, in my opinion, does five or six a year, that's quite a bit. You need to look and make sure all other conservative therapies have been exhausted. Dr. Neruz did a wonderful job of looking at patient selection. You have to look at contraindications and anticoagulants. We use eight contact leads, but I guess you could use a 16 contact lead if it was bilateral. Use the PERC leads, not so much the paddle leads. We usually, when we're placing these subcutaneous in the face, we use fluoroscopy and ultrasound so that we can place the lead in the right tissue plane, which is typically subcutaneous. Trials, depending on the physician, I like a seven day trial. As Dr. Neruz said, you need a 50% reduction in pain, increased activity, and possibly medication reduction. And we wait, I put two to four weeks because that's what the standard with like SES is. So I just kind of adopted that, but sometimes it's more around the four week interval to get these things approved. Since they're off-label use, a lot of insurances will not cover these. So you have to spend a lot of time trying to get them approved. And you may have to do peer to peers. You may have talked with the medical director, but in these truly refractory cases, it's important to be able to relay that to the reviewing physician so that you can get these approved. Just a patient of mine, these are very old leads because these are quad plus leads, and this is an octrode. These don't exist anymore, but this is a patient of mine who was hit in the face with a baseball when she was 18, and we had done all sorts of procedures and finally did some peripheral field stimulation. Another patient of mine was superorbital and infraorbital neuralgia from an injury. These are subcutaneous, your standard SES leads. This is for a superorbital placement. You can see the 14-gauge needle here. This is a superorbital foramen. The nerve is sitting here. This is a lead that we passed through because you can see the contacts here, here, here, and here, and also back here. So this allowed us to place the lead under the skin, above the fascial planes, and then stimulation. What you look for, you need to make sure that the anesthesiologist, I do these under general anesthetic, that the anesthesiologist does not give a muscle relaxant to the patient, because if they do, then no matter how much motor stimulation you do, you're not going to get a contraction because the patients are paralyzed. So please relay that to your physicians, your anesthesia colleagues, as you're doing these procedures. This is not a patient that I did, but Dr. Slavin showed a picture of the gasserian ganglion stimulation, deep brain, motor cortex, and the whole shebang. This is a patient, a picture I got from, I won't say who, but it's one, two, three, four, five, six, seven, eight, nine, there's 10 leads in this patient's face. I think this is going beyond what you really need to do. Sphenopalatine ganglion stimulation is out there, a company, this is a small electrode that has to be placed into the pterygopalatine fossa to stimulate the ganglion. This device is anchored onto the maxilla. When a patient develops a cluster headache, then they activate the device to abort the pain. Technical problems are lead migration, muscle contraction. If your lead is too deep, lead fracture. As you're placing it, it's a 14 gauge needle, so you could poke through the skin. Erosion and infection. Couple of patients of mine, this is just an extreme case where it was a worker's comp patient. We placed the leads. They started eroding through the skin, but the insurance would not let the patient come back to see us. So this sat like this for about six months where it eroded, healed, and finally we had to take it out. This is the patient that I showed that had the three leads. You can see part of my ENT doctor loops them, anchors them to fascia and tells them behind the ear, down to the chest. And this one lead was eroding. So he was able to open this up, take a single lead out, close back up and let that heal. So it is possible to salvage systems. We always want to know what the literature shows, but this is a great paper by Corey Hunter and Ajay et al looking at neurostimulation. The levels of evidence, it's really limited or consensus based for supraorbital for stimulation, infraorbital and for suborbital and occipital. For channel neuropathy, there's low level evidence. There's no evidence for trigeminal neuralgia, auricular temporal, level four evidence, high cervical spinal cord stimulation, level four and five evidence, peripheral nerve field, level four evidence and SPG for trigeminal neuropathy is a level four. And it doesn't show here really for persistent neuropathic facial pain as Dr. Norris was talking about and gasserian ganglion stimulation level four. So there is evidence, but it's low levels. Looking at the NAC guidelines using the hierarchy of studies by the U.S. Preventative Service Task Force, the levels of evidence are two dash three, which really shows that it's multiple series compared over time with or without intervention. And so it's a lower level of evidence. Excuse me, I need to go the other direction. For intracranial stimulation, the level of evidence is even lower. Most recently the Aspen practice PNS guidelines, stimulation like simple to nurse chronic migraine has a higher level of evidence and insufficient evidence recommends stimulation that's superorbital and for orbital nerves for neuropathic pain, it's a lower level of evidence. But I think what is important is that, as Dr. Rotz would say, lack of evidence and doesn't necessarily mean lack of efficacy. So if you choose your patients correctly, then I think there is benefit in these really refractory cases. Thank you. All righty, perfect. Thank you so much, Dr. Day. So the last topic that I'm going to cover today is the last presentation. It's regarding the advancements in emerging technologies for craniofacial pain neuromodulation. So this is like a ever expanding field like any other field in neuromodulation. We are getting new technologies, new type of waveforms and changing in the hardware. So what are the things that you, or drivers of the improvements? So in expanding in indications, like we are getting more and more new indications approved or evidence supporting the effectiveness of neuromodulation for craniofacial pain. And over time, the acceptance in medical community regarding the efficacy and long-term efficacy of these treatments are improving and expanding. And also we're getting advancements in hardware. One of the advancements that has been happening in neuromodulation and peripheral nervous stimulation for craniofacial pain is a wireless implantation. So these are like a smaller leads with a smaller IPG and they can be implanted in craniofacial areas. There are several case reports that has been reported for supraorbital and different craniofacial targets. And there's a case report particularly for supraorbital implantation for two octopolar wireless neurostimulation but successful improvement and pain relief for about 12 to 24 months. And this particular case report was about high-frequency stimulation. In our group, we actually presented a case review, a case series of our own institution and showed the wireless peripheral nervous stimulation for several indications, including occipital neuralgia, trigeminal neuralgia with the field stimulation for it. And we followed these patients for pain scores in PDI for about six months. And I about to publish the longer follow-up for these patients with significant improvement in PDI and pain scores. So the advantage of using these type of wireless stimulation is a smaller IPG. So definitely much less invasive procedure for the patient, especially in the craniofacial area where you implant the device. Sometimes you might not be having the luxury of tunneling all the way down to a lower back and you might have to use a different places like the interior pectoral area or closer to your upper extremity to implant it and having a smaller IPG, it will work for your advantage. And this location-wise and also the patients that will have a very small, like a smaller BMI. One of the new advances in neuromodulation, particularly for peripheral neurostimulation is temporary peripheral neurostimulation. This type of peripheral neurostimulation is implanted for 60 days to treat chronic pain. And so the effectiveness of it is a mechanism of action. It's sort of like a field of stimulation, unipolar stimulation inhibiting the alpha, delta and C fibers and also decreases signaling in the higher centers of the central nervous system. There are some reports of its utilization for occipital neuralgia. We have done several of the cases with this temporary peripheral neurostimulation for occipital neuralgia as well with good success. And also what Dr. Day mentioned, sort of like a recent development is like on-demand wireless microstimulators. And these are like patient can actively control as needed this type of stimulation. It's like for SPG microstimulation therapy, very good evidence behind it, used for episodic and cluster headaches, which showed potential overall healthcare cost saving within five years of post-stimulations and significant improvement in outcome. One of the new technologies in advancements in neuromodulation is the closed loop system. So it's the evoke potential feedback and it's extensive evidence has been reported recently for dorsal column stimulation for efficacy and improvement in outcome with patients with those types of indications. But in the future, looking at this, you'll see that there might be a huge advantage for craniofacial pain. The way it works that this automatically adjust the stimulation and levels to maximize the overall patient receives the optimal intrapeutic dose. It means that based on the patient's different changes in vital signs, physical activity, posture in the stimulation can adapt itself and keep the stimulation intrapeutic window. So at this point it's only used in dorsal column stimulation, but I wouldn't be surprised in the close future there will be some utilization and expansion of its indications for craniofacial pain. So the advances doesn't stop here. I think besides the smaller implantation devices, on-demand stimulations and positive outcomes with micro stimulation and temporary stimulation, I think using the new technologies like biomarkers and wearing devices that you can get and collect the outcome for the patients with craniofacial pain, it will take us a new era of helping the patients with craniofacial pain with neuromodulation. And of course, as Dr. Day and other colleagues mentioned, this is a treatment that it comes after failure of conservative management and other interventional treatments. All right. This is my daughter that she always probably, I hope that she's gonna be the future physician comes out at the end of my every single presentation as a tradition. Awesome. All right. Thank you so much, everyone. I'm gonna open the podium for the questions. And at the end, please remember that there is a brief evaluation forum that was shared in the chat box. Please make sure that to complete that, it will be very helpful for us to get the feedback from you all. I'm gonna start with a few questions from our esteemed panelists. And I'm gonna start with Dr. Nowruz first. Dr. Nowruz, great presentation in terms of patient selection. Do you think the value of the trial in converting to implantation? Is there any like, you think that it's a significant role to it compared to diagnostic blocks? We know the diagnostic blocks probably the only advantage of it it will be to choosing the target. But in terms of trial itself to predict the success of the neuromodulation in craniofacial pain, do you think that is any more utilization for trial or less utilization compared to dorsal column neuromodulation in this field? No, I agree with you. We don't have much evidence or published data at least to make a sound consensus. But we have now temporary, also temporary peripheral nervous stimulation leads. So definitely for those temporary peripheral nervous stimulation lead that you leave for 30 days or maximum 60 days, it doesn't make sense to do a trial, correct? So for those one, I would say definitely no need for a trial. The issue is we're practicing in this country and it's a requirement. I don't think any third-party payer or carrier will cover permanent implant without a trial. This is not a good reason just to put a trial, but you don't have other argument against this. The diagnostic block, for sure you need it as a part of the treatment, as a part to come up with a diagnostic plan. And then if it's intractable or lost efficacy or the diagnostic response to the block is short-lived, then you move on with the neuromodulation. I personally prefer to do a trial because it's an opportunity for the patient to try it. I mean, if the patient order something to buy, a clothes or something, they always wanna try it first. But the trial gives you an idea about tolerability. For me also, if you can capture the nerve or not, you capture the fissure plane. So you learn more about the anatomy of the patient during the trial. Although we have some experience in the occipital nerve stimulation community. And honestly, the subgroup analysis of most of the published data showed that with trial, without trial, the outcome might be the same, but unfortunately the outcome was not great anyway. That's why the FDA declined the approval of migraine for occipital nerve stimulation because the three RCT trials were more or less negative. But when they did subgroup analysis, they found no significant difference. But I will say the correct answer is a trial is required, but it does not mandate a better outcome for the permanent implant. Wonderful. Dr. Miles, Dr. Slavin, any points from you all? And also I wanted to know that any of the presenters have any opinion on using a staged trial for difficult cases instead of like doing the percutaneous trial? Yeah, I agree with Samer. I think over the years, having 25 years experience, 26, with looking at the first trials I've done coming out of fellowship, I had some cool stuff. If a patient said, yeah, I think I got 50% pain relief, like cool, let's put it in, because we're super excited. And then I look at my three, five, 10, 20 year, follow up on those same patients and thinking, well, maybe 50% wasn't enough. I think in my current experience, you walk into a room and the patient looks at you and they said, please don't take this out. Then most likely you will have a good outcome. I'm not saying you're gonna have 100% great outcome, but you'll probably have a better outcome if the patient says, well, I think it might, I don't put it in. And that's just from my own experience, my own follow-up in my patients. If patients volunteer information, I think there's a better chance that it's gonna work as opposed to trying to coax them into 50%. But I think the other thing that Dr. Nowruz was saying, you've gotta look at activities. You've got to look, you know, for somebody, like he was saying, he got 40% relief, but they said, oh my goodness, I can eat better, I can chew better, I can sleep better. I mean, those activities of daily living are so important that sometimes we overlook them and all we look for is pain relief. And also the comment that he made about, well, some of our patients take opiates for other reasons other than the pain we're treating. So we have to keep that in mind as well. So. That's absolutely correct. I feel, I totally agree. I don't know if Dr. Slavin can hear us if he has any comments and adding points, but I totally agree. I think it's an overall combination. I have seen that sleep quality being a very important factor for the success of the trial and in general for neuromodulation, particularly for patients with occipital neuralgia and trigeminal neuralgia. And even for trigeminal neuralgia, a lot of times, some of my patients are like, you have difficulty even eating. So when they come back and say that, oh, it was so significant that I was able to eat well with no fear of having the painful episodes. So it's been like finding what is the trigger. And you see that if that trigger during the trial actually changed, their quality of life will be important. My last question to both of you and Dr. Slavin is most of the neuromodulation options that we have, they are off-label. And because they are off-label, the MRI compatibility, it might be a significant limiting factor in these patients. I personally always have a long discussion with patients that understand that this if you need MRI, so there's a very good chance that you might have to explant this device for you and make sure that they have a greater understanding. Do you both see any in the future hope that maybe some unlabeled studies will come in some of these devices, particularly for craniofacial pain become unlabeled and more access for the patients and less chance of having trouble with the MRI. And we know that the smaller patient population and probably not as big of a desirable market for the neuromodulation industry to invest on it. But I would like to know what is your opinion and how you approach with your patients when this question comes up, especially with patients that it might be a chance of getting the MRI in the future. So, this is a tough question. I mean, Dr. Day, if you don't mind, I can start. Yes, that would be wonderful. It's a tough question because the lead is very close to the brain, which when I do MRI later on, so it's not like even have a conditioned approval, you have a lead in the low back and you can do MRI of the brain. So, definitely, I'm very reluctant to offer craniofacial neuromodulation, for example, for patients with MS, because they will require frequent MRIs. And I have, I had explanted patients because they needed an MRI. So, you have to take it out, accept the nerve stimulation, and it was helping with their headaches, but the headache got worse or there's something that require MRI. So, it's an informed consent. The patient needs to be educated also before making an informed consent. And it's pros and cons. The good thing that it's, it looks minimally invasive, which it is minimally invasive because it's always subcutaneous, but I don't want to downplay it. It's minimally invasive. So, if you need to explant it, I did, and actually after the MRI, one of my patients really begged to have it again. It's, although it's percutaneous and looks very easy to put meticulous attention to detail is extremely important. Migrations are very common. You think you're going to do it, you put the OR for 30 minutes because it's two leads under the skin, it's easy. Actually, positioning and shaving will take an hour. So, it's something elaborate. But the morbidity associated with it, yes, it's very low because, I mean, if there is infection, usually it's subcutaneous, if there is infection, usually it's subcutaneous infection. We are not talking about the gazillion ganglion or the deep pterygopalatine fossa stimulation. But the MRI is always and always a thorny topic that if the patient is aware of it, and if we need to explain, usually they are not upset because they made a decision to proceed with it knowing the limitations. Hopefully, some of them now they are MRI compatible, but again, conditioned and not all the radiologists are comfortable. So, we need some work on it. Maybe Dr. Day or Dr. Slaven have more updates about the MRI compatibility of the peripheral nerve leads. Yeah, I think, you know, I guess the good thing is in the generators, if you had to explant the leads, you can leave the generators in because you wouldn't have to remove those. And that's the biggest cost of the system. But I agree with Sam when he was talking about MS, you always have to look, is this patient going to have an MRI sometime in their life? Even though some of the leads systems we use are MRI compatible, well, that's, the leads are MRI compatible in the epidural space, not peripherally. Now, 20 years ago, did we MRI people with old systems? Sure. We send a fellow down there who would sit with the patient to make sure nothing bad was going to happen. But, you know, talking with the patient, explaining the patient, especially saying it's off label. I think a lot of things we do, we don't, we just, because it's normal for us, we don't tell the patient, oh, by the way, this is an off label use of the system. We don't document that. And we need to document because we doctors keep telling each other we need to document, but then we don't. And then if we have an untoward event, then that comes into play. But Constantine, what do you think? Constantine, you're, you're still mute. We can't hear you. Now, can you hear me now? Wonderful. Yes. There are some devices which are considered to be reasonably MRI safe. There are some wireless devices, but they're still not on label for craniofacial use. So you have to keep that in mind, even though there are plenty of anecdotal studies of patients who had the devices and had their MRI and nothing happened. I have nice illustrations of this, but I still don't recommend my patients getting it because if something goes wrong, there's really no protection. Then everything we do in this reality is off label. The manufacturers will not protect you. And the radiologists will take major risks. So, so I think it makes sense. I agree with mentioning about patients who need MRI, try to avoid devices, which are not approved for that or get an MRI just before the implantation. So at least you have some time before they may not need it anymore. Because one thing we didn't talk about is that in the craniofacial pain, there are cases when patients have their devices removed because they are not needed anymore. And that's something that is rather unique for this. Because not because they don't work anymore, but the pain eventually disappears. And when that happens, that's a great example when we were able to help them without destroying it. So that's what I like about neuromodulation in this regard. And I'm sorry about the noise here. So it's, I'm reading an airplane. Sorry. You're good. We can't hear the noise. You can't hear the noise. It was very real time. And I will tell you regarding the efficacy, I had a patient that this is kind of like a hard to see in other type of neuromodulation. And I had a patient of occipital neuralgia in one lead occipital neuralgia and chain for battery change after nine and a half years, because she just realized that the pain is not covered anymore. And you just change the battery for her. So this is really hard to see in like other types, but it's like a lot of successes in craniofacial neuromodulation. And my favorite, I don't know how it was like, but my favorite is actually occipital neuralgia. I see a lot of success with occipital neuralgia personally. Yeah. I have a colleague who, cause I was always thinking about this with the DRG stimulators about using the DRG lead to stimulate the caesarean ganglion. And I was thinking about that and a colleague of mine in Brazil actually did it using the same parameters for DRGs for the caesarean. And I had some pretty good relief from it. I think if I could find a way to keep those leads anchored and they don't move in and out of foramen, that would be great. But I have a question to you guys when it comes to like post-therapeutic neuralgia in V1, it's like the last three stimulators peripheral field stimulators I placed, the patient's got no relief with PHN. What is your experience with that? The same. This is, I think, one of the most difficult neuropathic pain to treat. Everything works for them just temporarily. We put the supraorbital nerve stimulation, they like it for two months, three months, and then for some reason does not last long to the point that I don't offer it. Honestly, I don't offer it anymore for post-therapeutic neuralgia. Yeah, I think that's, you know, my last three cases were specifically that and they got no relief. They got a little bit early, but none, but I really haven't seen that in the literature, you know, the failure of peripheral field for, you know, PHN. And so I'm actually thinking about publishing them at least to get some information out there. So like, Samra, you stop doing it. I'm going to stop doing it. I don't offer it anymore. Palatine, I don't know your experience. I do it rarely. The first published report of supraorbital stimulation was on a PHN patient that came out of neuromodulation, I think in 2002, and actually worked quite well for that patient. But in my personal anecdotal experience, it's kind of hit or miss. Some people like it, some people hate it. So I still offer it to patients. I try it every now and then, but it's not the best indication in my opinion. Yeah, I think I had a few patients on the V1 distribution for like a Ramsey-Hahn patients, no success with those. The only patient that I can remember that I had a good result, it was occipital neuromodulation. It was like a particularly occipital area, and that patient responded relatively well. But I think it's for the facial pain, mostly the success is not that great. Post-traumatic, yes. I would put supraorbital. Actually, it works very beautifully if there is peripheral nerve entrapment or peripheral nerve irritation or injury, whatever you want to call it. Yes. Frontal sinus surgery, I have a patient with a horse kick. Yes. Cluster headaches, yes, because usually V1, sunk head V1, hemoclinic continual V1. But for some reason, I agree with Dr. Day, post-therapeutic neuralgia, maybe because we see them already two, three years after the fact, it becomes more centralized pain. Again, to the point that I don't even bother to offer it anymore. And it makes sense. Probably the reason is it's a central, it's not a peripheral indication. Right. So, but great discussion. Thank you so much, Dr. Nowruz, Dr. Day, and Dr. Slavin. I'm sure it was very educational for our audience. I personally learned a lot from your expertise and wisdom for craniofacial neuromodulation. We're looking forward to more discussions in the future. And thank you so much for supporting this webinar to make it a success. Thank you. Thanks for having me. Thank you. Good night.

craniofacial pain management

neuromodulation

Dr. Slavin

Dr. Nourouz

Dr. Day

mechanisms

patient selection

treatment types

individualized patient expectations

central neuromodulation

peripheral neuromodulation

diagnostic blocks