Transcript
Question: Dr. Callen, there’s two questions about access to care specifically that we talked about that came up. So maybe we can start there. One from a patient says, “Is there anything that we can do as patients to help with the insurance codes problem that you’re having? How to get better coding for the procedures that you, that Dr. Madhavan, and everyone are performing?”
Answer:
Dr. Callen: I wish I knew a very specific answer to that, because if I did, I think I would be trying to advocate it for us now. I think that engaging health policy experts and other sort of—this has happened in other diseases where we’ve needed to refine our medical coding and medical language around other disease states. I’m curious if any of my other colleagues have ideas on ways that we could begin approaching this or advocating for this in general, but I don’t have a great answer for it.
Dr. Madhavan: I’m with you, Andy. I think it’s a really hard thing. I mean, one of the things we don’t learn in med school is how to deal with this kind of stuff, right? So I have generally relied on experts, and that’s where folks like people in the Spinal CSF Leak Foundation are so helpful, but it’s really tough.
Moderator: Thank you. I think patients really want to contribute in any way they can to making it easier for you, which therefore obviously makes it easier for us, too. But the systems are often really complex, and I know they’re quite different in different countries. Dr. Beck, I’m curious if this comment that we made about the coding systems in the States with the ICD-10 codes, is that something that exists in your system, or is it quite different there?
Dr. Beck: No, absolutely. That’s a huge problem. And I think the lack of centers that take care of spinal CSF and PDPH patients is truly related to this. And I know many centers who tried to start a CSF leak service, but they failed because, as Dr. Callen has said, you get the same amount of refund for a standard myelogram that takes probably 20 minutes versus one that the chairman of the neurology department and radiology department needs to do, takes one and a half hours, and redo the scans, and so on. So it takes too much time for many busy services to start a CSF leak center, despite there being this huge will. And I really do not understand this, because the caregivers, not the caregivers, the funders of the system, they should have an interest in pushing this, because many, many of the affected patients are losing their jobs and are a huge socioeconomic loss for the society. And this hasn’t really been understood, I think. And this conference is a start, and we need to push harder to convince the funders to fund this type of clinical care as well as research better. It’s a huge problem, and I fully agree.
Dr. Callen: I think that one thing I’ll just add to that, I completely agree, Jürgen. And we’ve kind of talked about this touchy-feely part of, we can learn from each other, but I have learned so much from my patients, who, I am surrounded by doctors all day. I’m a doctor, this is all I think about. I am embarrassingly ignorant of things about economic policy, healthcare system-related issues. And I have patients who I’ve approached me after this conference who were like, “Actually, that’s my thing, that’s my job, I could help with this or that.” And this is the sort of tangible teamwork that we can create and foster together, is that we are very siloed in medicine and we love, we’re just focused on this one thing, but we need broader perspectives, especially from people suffering from the condition, who may have expertise that we don’t, that could help us together advocate and push this field forward.
Moderator: I think that there’s a lot of patients that would love that as well. Just from a practical perspective, you all see patients with multiple different comorbidities, for example a connective tissue disorder or a mast cell disorder. I asked Dr. Callen earlier, when we were prepping for our conversation, what would he be amenable to a patient, let’s say bringing sort of a PDF from a specialist to help kind of inform some of the care that he’s doing. On that level, I think that’s something that patients aren’t really sure where to navigate themselves, not wanting to be too pushy, but having these other comorbidities that exist. I’m curious with the other physicians, Dr. Madhavan, you’re doing scans for people. Let’s say they have contrast allergies. Are you open to those sorts of, not an official peer-to-peer, but if a patient was to bring you a PDF that their other doctor presented to them for this sort of procedure?
Dr. Madhavan: Yeah, I certainly am. I think it’s super helpful because a lot of times we don’t know their perspective going in. We don’t know what they’ve been told. We don’t know what they know about the procedure, and things like that. So, I’m very open to that. I think what I could anticipate they would run into, in some cases, is somebody might be really having a really busy day, and that could be what could prevent them from doing stuff like that. But I never think it hurts to try. I think it’s just a good idea to come, like you said, with as much information as you can. I don’t think you should ever have fear that your doctor is not going to be receptive to it, because if they’re not, then it’s kind of on them.
Moderator: Fair enough. Thank you.
Dr. Callen: I think that, you know, if you do enough of this work, you begin to be humbled by how much you don’t know. I tell my patients, I’m not an expert on mast cell activation syndrome. I’m not an expert on connective tissue disorders in general. And it’s easy, I think, as a physician, you know, we like being experts on things and we don’t like saying we don’t know things. And so it’s easy to say, well, if I don’t know anything about that, then that must be something that is not real, or what have you. But all it takes is taking care of enough of these patients to see somebody have a severe skin reaction to just ChloraPrep on their skin to know this person has more of a hypersensitivity than I realize. There’s something to this that I don’t fully understand and that medical science doesn’t fully understand. And it’s this repeated pattern of my patients having these issues, these systemic issues, there’s something here that we don’t fully yet grasp. And so I think it’s just always important, as soon as we start feeling too confident in what’s going on, I think we start to sort of fail ourselves and our patients when it comes to those issues.
Moderator: I mean, I was one of those patients, right? I didn’t know I had MCAS until I went into anaphylaxis on the table during my fourth round of patching. But I ended up having symptoms of it for many years. I had all these weird reactions or all these weird things happening in my body that I just never thought to connect. But it was reactions during the procedure that sort of precipitated the need for that diagnosis. I think some patients are finding similar, where they have these underlying issues that they didn’t know about, and during the procedures there’s some sort of reaction that’s causing them to investigate further. So it’s sort of happening in tandem.
Question: For one last question on that front, there’s a question we got submitted ahead of time about if a patient does have a comorbidity such as MCAS, and I don’t know if Dr. Schievink is still here, but I’m sure he has thoughts on this too. If their body rejects a dural graft or may reject a dural graft, is there a sort of better graft or a graft that has more tolerance in that patient population versus another, or a type of repair that is, let’s say, more successful to patients that may have those immune system disorders? I don’t know if Dr. Beck, you have a thought on that question.
Answer:
Dr. Beck: There is clearly one thought it is using PRF more often. PRF is platelet-rich fibrin, which is just we withdraw blood from the patient and centrifuge it in the OR. It takes like 10 minutes or so during the procedure, and it depends on how we handle the vials. We can make fluid PRF or rigid PRF formulations, and this is only from the patient. There is no additive, no nothing. And this, I think, is at least from theory probably a good way for MCAS patients, but there are no data yet out. But this is clearly something I would try.
Moderator: Do you find that reactions to TachoSil are less than, let’s say, a bovine graft, for example, or is that not something you’ve sort of seen a pattern for?
Dr. Beck: No pattern. Sorry. No pattern.
Moderator: No problem. That’s fine.
Dr. Beck: Reactions to both. But I have to admit I haven’t recognized a specific pattern for that. Sorry.
Moderator: No, don’t be sorry. We’re just happy to have these conversations with you. Dr. Callen, are there any efforts in the United States to do something of the nature that Dr. Beck is saying, of sort of that centrifuge of our own fibrin as an opportunity to sort of sidestep the hyperactivity for some people?
Dr. Callen: I’ve heard of some physicians doing things similar to that. I know also, just speaking from personal experience, what we’re doing here in Colorado, we’re working closely with some of our PhD collaborators who are working on hydrogel-based dural substitutes, which theoretically have less immunogenicity in terms of reaction. That’s still a fluid material, but the nature of hydrogels could theoretically be less inflammatory or immunogenic, so to speak.
The one thing I learned from speaking to more surgeons and working in this domain is how frustrated they are, at least in the United States, with the lack of options for dural graft or dural substitute. They all have something good about them and then something bad about them, and then you have to choose which is the one that you’re going to use for any given procedure or surgery. So I think there’s definitely more work to be done, and I think an enterprising medical device company could really make a big difference here by helping in this way.
Moderator: Thank you.
Question: We’ve talked about normal imaging for today in many different sessions, and I’m wondering, as patients are wondering, regardless of the type of leak, is there a theory as to why this image appears normal? We know sometimes in chronic cases it resolves into a more normal state. For leaks that are already appearing as normal at onset, is this because there’s potentially underlying higher CSF pressure or volume? Or is there a known mechanism for why imaging would appear normal versus not?
Answer:
Dr. Madhavan: Sure. Yeah. I mean, not specifically that I know of. I think you’re right that many times it seems to happen in patients who’ve had a leak for a longer period of time, but not always. I’ve also seen it happen in patients with relatively recent onset symptoms. I think it probably has something to do with just a normal compensatory mechanism. Jürgen, talked about that editorial from Jeremy [Cutsforth-Gregory], and I think that highlighted a lot of good points about how there’s some sort of compensation with the way the structure and function of the dura that probably causes the findings of intracranial hypotension to improve.
And the other side of it too, I think you’re mainly referring to brain MRI findings, but more and more I’ve started to appreciate even spine MRI findings in patients with dural leaks can normalize or be normal too. So this whole concept of just brain and spine being normal, I think, is really important.
Moderator: Thank you. I think we’re all realizing in all these conference talks there’s so much, it’s a nascent field. There’s so much research that happens, and there’s more research, obviously, that we are excited to see done.
Question: Speaking of, one of the questions we received is, is there a known association between menstrual symptoms and hormone fluctuations that modulate CSF? There were studies this year that came out about how the menstrual cycle affects CSF production and flow, and that of spinal CSF leak symptoms, and the question was, are there any studies planned for spinal CSF leak physicians, especially given that the condition affects women a lot of the time?
Answer:
Dr. Callen: I’m woefully uninformed on this specific topic, and I think this just points to another reason why we need better multidisciplinary collaboration, so we can have, for example, endocrinologists weigh in on this topic and give their opinion about this. I mean, I know that menstrual cycle and hormonal fluctuations can definitely modulate other headache disorders, and contrary to what doctors love to believe, which is that every patient just has one diagnosis, you can have more than one thing going on. One thing can modulate another. People can have spinal CSF leak and something else too, and those things can interplay and make each other worse, for example. But I don’t have a good answer or really any nuanced insight into that specific question.
Moderator: Thank you.
Question: Throughout the conference today, there were several instances and questions about timing and how timing for treatment matters. In general, patients often ask about the long-term effects of a spinal CSF leak that goes untreated. We’ve seen Dr. Schievink presentations about superficial siderosis and other complications thereof. But one question that is asked often and was asked prior to this conference was whether patients can incur TBI-like injuries if there’s a lower volume of CSF that’s cushioning the brain. There is an overlap in the two symptoms, and patients are wondering, does it actually damage the brain in the way a TBI is seen to damage the brain?
Answer:
Dr. Beck: I’m getting a more and more strong opinion on that, and I think really a CSF leak needs to be repaired. What we are speaking of right now, superficial siderosis or the atrophy of the muscles, is just the pinnacle, the tip of the iceberg. I do not believe that a spinal CSF leak is good for your brain or for your spinal cord, and there’s more and more data that we have. This is a very controversial term, but this kind of spinal dementia, a very, very exuberated term. Brain fog, on the other hand, is real, and we can measure it. The latest data from Freiburg is that we only needed 40 patients or so and did simple tests before surgery and two days after surgery, still with anesthesia in place, and they all were dramatically better on cognition tests and set cause performing just simple tests. So there’s a lot going on, and the spinal CSF leak is not healthy for your brain. I haven’t thought about this, but I do even like the comparison to traumatic brain injury.
I think it is also, again, the tip of the iceberg is the behavioral variant frontotemporal dementia, where the brain really sags down immensely. But there’s also a tiny shift in between the brain when we measure it. We call it tectonic shifting. The mesiotemporal structures are displaced before and after leak closure, and the mesiotemporal structures are clearly related to cognition and to memory. So I do really believe a spinal CSF leak needs to be closed.
Dr. Callen: Sorry, Jodi, I just had a follow question for Dr. Beck. I was really impressed and interested in what you were talking about in Amsterdam about your group’s work. I just saw your comments about subdural hematomas and thinking about them, and how many patients are misdiagnosed in terms of having subdural hematomas. If we just go looking at all people who have subdural hematomas, what percentage of them have a spinal CSF leak? I think it’s sort of tangentially related to the question, in that this is something we think about as trauma, or traumatically caused, and then also think caused by spinal CSF leak. Maybe you could just tell us one or two things about that?
Dr. Beck: Thanks for this question. Of course, I love to talk about that. So we started a prospective study, even registered, that we do on all patients with chronic subdural hematomas. We do an MRI and a myelogram with a suspicion for a CSF leak, even in [patients] 85 years old with a known fall. Currently, the numbers are not official yet, but it’s not a blinded study, so I can talk about it. It’s prospective but not blinded, and currently the numbers are in the range of 10, 12, 15 percent.
This is one of the most often happening diagnosis in any neurosurgical center around the world, is chronic subdural hematomas. And if we really do detect spinal CSF leaks, and you only do one shot, not all the sophisticated stuff in elective cases, and if one-shot, one myelogram is enough to detect 10 to 15%, this is changing the story. And we are a little bit afraid of our own results, because what’s next? Shall we really scan all patients with chronic subdurals? It’s a big issue.
And this also underscores only that we really do need a biomarker for CSF leaks. We do need a biomarker apart from imaging, something that we find in the blood, something that we find in the CSF. And this is probably the next big, big trial we should do.
And talking about trials, this is funded by my department and by the department of Horst Ubrach, the radiologist, and Niklas Lützen and Charlotte Zander, and we do not get funding for this. Imagine we complained about education and people getting to know CSF leaks. Imagine that CSF leaks have the same incidence like multiple sclerosis, which is a multi-billion dollar industry, and we do not get funding for a single study. So there is really, let’s put it in better words, there’s way of improvement. Yeah.
Moderator: Thank you.
Question: This is also a question for Dr. Beck, specific to the neomembranes that you have talked about today and otherwise. Given the presence of angiogenesis of those neomembranes, patients are wondering, can ongoing CSF leakage damage the integrity of the dura surrounding the leak? Like, is it common that around the leak it’s sort of translucent or thin due to CSF being outside of where it’s supposed to be? Does it have a corrosive component?
Answer:
Dr. Beck: Good question. No, I think it’s the other way around, but this is only from my surgical experience. I think these neomembranes form and try to strengthen the dura. They don’t do it, but it’s not a corrosiveness of the dura. It’s just an additional layer. So, I think from my perspective, you don’t have to be afraid of an additional corrosion of the healthy dura. It’s just the spread of a faulty attempt of the body to heal it, like in some autoimmune arthritis. It’s overshooting. It’s not corroding the dura. It’s just an additional layer that is too much, and it is usually one and a half levels above and below the leak, and then it fades out.
Moderator: Thank you.
Question: A question just generally about CSF lymphatic fistulas. I think, first of all, for those patients who aren’t aware, if you could first explain what they are versus CVFs and just explain what makes them different to CSF-venous fistulas, as they’ve been discussed in some of the literature today as well, and not all patients are familiar with that type of leak.
Answer:
Dr. Callen: Yeah, I mean, I could start with this, and then Ajay, if you want to jump in. It’s been a much more rarely described phenomenon, and it was, I believe, Dr. Lützen and colleagues who first described a case report of it. We’ve also seen and published on a person who had a CSF lymphatic fistula very close to her skull base that resulted in a syndrome of intracranial hypertension.
And one thing that I’ve observed, and I’ve spoken to my colleagues in Switzerland and Germany about this, is I’ve had a couple cases where I’ve had a patient with a dural tear, a type one leak, very sort of bread-and-butter, and on the delayed myelogram I’ve seen uptake of the extradural contrast into the thoracic duct near the lymphatics. So this is not necessarily a primary CSF lymphatic fistula or leak, but it then makes me wonder if this could be naturally resorbed into the lymphatics via the epidural space, and there’s a conduit between the two. Are we potentially missing some leaks that are potentially, in some way, secondary CSF-to-lymphatic fistulas in that way?
I do think, like with the CSF-venous fistula when it was first described, it was, oh, this is this incredibly rare thing, we’re never going to see this, but maybe we just don’t have the tools yet to really see it. And perhaps it’s not super common, but I think that it certainly is out there and deserves attention.
Dr. Madhavan: Yeah, interesting point, Andy. I agree with all that. I think that the one thing I’d add is that there’s kind of two, in my mind, two different distinct types of this. So Dr. Lützen had this nice, interesting case of a direct CSF lymphatic fistula. So that’s kind of analogous to a CSF-venous fistula, where it’s going directly from the spinal CSF space into the lymphatics. And then there’s a different subset that’s been described, which are related to congenital lymphatic malformations. So these are things that you’re born with, and they just happen to occur close to the spinal canal, and that results in CSF leakage. Both of them, I think, are relatively uncommon, but I completely agree with Andy. There’s a strong possibility that we just don’t have the tools to recognize a lot of these. So it’s an interesting topic.
Moderator: Many of these are interesting and sort of moving quickly. It’s really exciting as a patient to be a part of a conference like this, where I get to hear about the newest research and have the honor of asking questions too.
Question: One of the questions we received is about rebound intracranial hypertension. Basically, a question of different physicians have different opinions. Is it best to let your body recalibrate post-seal by itself, or to use something like Diamox or methazolamide or other medications to basically avoid putting pressure on the newly sealed leak site? And as a patient with a connective tissue disorder, I wonder if that answer would change if someone has EDS or Marfan or a disorder where their scar tissue may be different to the average patient, for example.
Answer:
Dr. Callen: I think my perspective on RIH has changed a lot. And I think when I talk to patients about it, I sort of frame it in the way that I’ve thought about it over the years. And I think when I first started doing this, one way that patients frequently conceptualize RIH is like it’s a good sign, like there’s a leak somewhere, the fluid’s been trying to be produced to keep the leak even, and then we closed it. So it’s overflowing. So, good, I got my rebound hypertension. But the evidence doesn’t really suggest that the presence of rebound hypertension is associated with treatment success. We’ve had several multicenter studies on different kinds of leaks, and none of those have borne out an association between RIH and eventual leak closure. And so, based on the evidence we have now, my opinion would be no, I don’t want you to experience symptoms of RIH. At its worst, it could lead to vision loss, which could be permanent, or nausea and vomiting, which that Valsalva could stress our attempted leak repair, and just general discomfort and pain, which I don’t want you to be undergoing at all.
I think surgeons, when they do, for example, skull base surgery, will place a lumbar drain to take the pressure off the site to allow the skull base leak to potentially heal. There’s an interesting question to be raised. I know that Dr. Simy Parikh, who’s now at Emory, has suggested that patients preemptively start Diamox before a treatment to sort of lower the pressure in preparation for the patch. I think that’s a very interesting question and one that we should do a study on, a trial on, and I don’t really know. But those are my heuristics in terms of how I think about it.
Moderator: I actually did do that. I asked my, I think I phrased it as, can I pregame my methazolamide before my patch, because I went into such severe RIH during my earlier rounds. And I was sealed on my third round of patching, but then it blew, and they said the same. We don’t have data that suggests it’s a good or bad idea, but I don’t think, other than making you feel terrible before your patch, sure, give it a try. And I ended up starting it three days before and felt absolutely horrible. Did that help keep me sealed? I don’t know. But it was something I tried.
Question: I’m wondering as well, when we look at the sort of brain sag discussion, that pressure, that pulling down, for the patients that have those classic symptoms, what structures are sending those pain signals? Or is this a better question for a neurology conference instead? Can you have – is it low CSF tractioning your cranial nerves or other nerves, or are there other mechanisms at play?
Answer:
Dr. Callen: I think, I mean, I could provide sort of not a good answer, but a sort of interesting question in response to that question, which is, I thought that maybe a slightly, I wouldn’t say overlooked, but there’s so many CSF leak papers that come out now, it’s hard to keep on top of everyone, but one that I found one of the most fascinating was the one that Duke put out that showed the lack of correlation between symptom severity and Bern score. And so, just to summarize, they found that having a more severe brain MRI did not correlate with having more severe symptoms as measured by standardized headache metrics, right.
And so this is very interesting because we always hear, oh, it’s sagging and traction on meningeal layers, sagging and traction on meningeal layers, or cranial nerves, right, but clearly it’s not as simple as that because if that was the case, the more brain sag you had, the more your symptoms would be. And so I thought this resonated with me because I would see people with a brain MRI that looked horrible, like I would expect them to be in a coma, and they’re sitting in front of me talking, and other people with the most subtle venous distension and nothing else who are basically bedbound. And this is something that requires a lot more research to understand what exactly are the pain-generating mechanisms for this.
And I think there probably is more to it on the venous side than we realize, in terms of the sort of nociceptive input from venous distension, from abnormal venous distension, or the body’s attempt at venous distension in the absence of appropriate venous capacitance or compliance. But I don’t have a great answer.
Dr. Madhavan: I can’t remember, was this from one of your papers? I remember there was either from a lecture or one of your papers, there was something where you were looking at the type of abnormality they have on their brain MRI, correlating that with the symptoms, like whether it’s dural enhancement versus brain sagging or something else. Am I thinking—
Dr. Callen: Yeah. Yeah. No, I mean, so I presented some of our preliminary data in Amsterdam, where we were, I mean, and we’re still going through that and hopefully going to get it out soon. But we were looking at, we had found in a previous paper that when you measure the elastance curve of a patient’s response and pressure change when you infuse saline, that correlated very much. If they had a low elastance or high compliance, meaning I put in five cc’s of saline but pressure doesn’t go up at all, right, that was more correlated with the presence of the Monro-Kellie findings on brain MRI, dural thickening, venous engorgement, subdurals, whereas the opposite was not correlated with the presence of brain sag.
And then we were looking more specifically, not at, and also then in our CSF-venous fistula clinical paper, the presence of those findings weakly correlated with the classic phenotype of disease, of the Monro-Kellie type findings. And then in Amsterdam, I mentioned that we were looking at patients who don’t get better, right, who we, the leak as far as we could tell is resolved, the brain imaging is resolved, but they get no better. And we were finding a very strong correlation between people who did not have venous distension on pre-treatment imaging and not getting better.
And so I think there’s something, this is why I continue to go back to the venous side of things. The body’s compensatory ability on the venous side to balance what’s going on on the CSF side, I think, is very important in terms of the symptomatology.
Question: We are at time, but if it’s all right with you, I could ask one more question that we get frequently, which is, do you have patients who have spinal and cranial leaks at the same time, and is there a place that, let’s say, treats both? But is that something you’ve seen in the patients you’ve treated, that they have both together?
Answer:
Dr. Madhavan: I’ve not specifically seen it. I think that, in general, they’re both rare enough that I think we only see them independently, but I don’t know if Andy or you have seen that before. It’s an interesting question for sure.
Moderator: Is it possible to have both together, I guess, is the secondary question that some patients ask. If they have, there’s been discussion of fluid coming out of your nose, not ears but nose, with a spinal leak, and some patients are told this is a part of the lymphatic drainage due to the traction on nerves. But for patients who do have positive beta-2 transferrin tests, could they also have a spinal leak at the same time, or is there some mechanism that would kind of preempt one or the other, is the question we received.
Dr. Callen: I think that most of the time the drainage from the nose is an autonomic response to the spinal CSF leak, a secondary dysautonomia that occurs in response to that. I would say I have not really seen that, no. I have not seen a bona fide, like a proven skull base leak at the same time.
I have patients who have had IIH definitely, with skull base skull-base meningoceles or pits, for example. I have a lot of patients who’ve been told that they have that. And while trying to keep an open mind, I have to ask myself if this is really going on so much. I mean, look at the AJNR website every single week. There are 10 new papers. We’re all so excited to share this research. Where is the peer-reviewed research that could show us this? Because if that’s going on, if we can make these diagnoses in our patients, and this is a phenomenon that is occurring so frequently, then we need to see it so we can help these people more.
And so I am very open to the idea that it’s possible. I just hope that people who are making this diagnosis, and patients who I eventually see, will share that information with us in a way that we can all see and hopefully help people who are suffering from that.
Moderator: Thank you. Thank you all for participating in this final Q&A. Dr. Callen will say some closing remarks, and then I will say some closing remarks, and then we will officially close.
Dr. Callen: All right. Well, I want to keep it short. I don’t want to go too long, a dramatic speech, but first I just want to say thank you all so much. Not only to my co-planners, my colleagues in the Spinal CSF Leak Foundation, who really taught me so much and sort of reinvigorated my drive for this work, my passion for this work, but thank you to my colleagues. I mean, Dr. Beck from the other side of the world doing this later at night, all of my colleagues giving their time to do this on Saturday.
I hope this shows to all of you, patients and patient supporters in the audience, how dedicated this community is to helping, even when we don’t have all the answers. I think that the talks today and this conference in general are just a really beautiful example of how far we have come in just a few short years.
As frustrating as it can be to have to navigate a system that doesn’t have all the resources in place, we are able to do things like this, to come together, to advance the science, to have challenging conversations, and really see each other in ways that I think have tangibly advanced this care in so many ways. And so that’s it. Thank you so much for your time, your energy, your commitment. Please don’t give up, to any of our patients who are suffering without an answer. Please don’t give up to my colleagues who are doing this work for maybe not the appropriate sort of coding reimbursement or recognition by your hospital. These sorts of things are what make this work worth it. And we’re going to keep pushing forward, and I can’t wait until next year when we have even more exciting discoveries and developments to talk about.
And so I will hand it over to Jodi to give some last closing remarks. But thank you all from my side, and I look forward to seeing you next year.
Moderator: Thank you. I feel just as effusive about the participation from the physicians in this conference. A big thanks to Dr. Schievink and Dr. Beck and Dr. Madhavan for donating your weekend and your time and indulging our great curiosity of all the questions that we’ve received.
I think this field has patients that do a lot of research. They’re curious. They want to learn as much as possible. They really want to understand the nitty-gritty of the field and what’s happening, and the research truly is really fascinating. And we appreciate that you’re here and willing to answer those questions and present on aspects of the field that you’re deeply involved in.
On behalf of the Spinal CSF Leak Foundation, we’d also like to greatly thank Dr. Callen for his curiosity and his desire to have patients involved in these kinds of presentations and partner with us for this unique conference, and have discussions that are a little different from ones that would normally be had at a conference.
We’re going to be finalizing that survey that Dr. Callen referred to and sending it out, and we look forward to everyone’s answers to contribute to research as well. And we look forward to seeing you next year.
Thank you everyone for taking the time to listen, to ask questions, submit your patient videos, and be a part of this collaborative experience. We hope you have a good rest of the weekend.