Moderator:
I’m sure many of you know the folks who are on the stage, and if not you will in just a moment. But the foundation has been very fortunate to work with leaders around the world, and those included on the stage. Nancy Sicotte is the far left, Jeff Bennett, John Rose, May Han, Maureen Neely, Michael Levy, and Ardith Courtney, coming to the stage now. This session is really all about you. It’s meant to allow you to ask questions, get answers, and maybe we could just start, Ardith with a very brief introduction of yourself for those who may not know you, yet. There you go.
Ardith Courtney:
How about now?
Moderator:
Yes.
Ardith Courtney:
Yes, there I am finally, brief introduction. I want you guys all know that you’re naked right now. You’re naked. I’m still dressed as you guys are naked. That’s how I’m imagining things. I am at University of California, Irvine. I was introduced to NMO by my colleague, Dr. Benjamin Greenberg, who was at Johns Hopkins and he came to join us. And through Martha and Maureen and some other people who I’m sure are here, I learned myself, and I’ve been trying to spread the word to the people who don’t know so you guys are recognized early, but I’m happy to be here and thank you for coming.
Nancy Sicotte:
I’m Nancy Sicotte. I’m the Program Director for the Residency Training at Cedars Sinai as well as the Program Director for our MS program. I see my role is one of education in particular and patient care. We’re trying to smarten up the next generation of neurologists. So they’re aware of NMO, that they know how to diagnose it, recognize it, and treat it. And so I’m really pleased to be here. Again, I think I have a few folks in the room that I take care of. Thanks for being here. And looking forward to a fun day.
Jeff Bennett:
Good morning everyone. I’m Jeff Bennett. I’m from the University of Colorado. I thank you for the view people. It’s a pleasure to be back for yet another patient day and I look forward to helping to answer some of your questions this morning. In addition to taking care of NMO patients and having a practice in a broad group of neuro immunologic disorders, I also practice neuro ophthalmology. And part of my job in doing that is not only taking care of vision disorders from problems in the nervous system, but educating my fellow neuro ophthalmologist on the recognition of this rare disorder, which sometimes can be delayed if it’s not recognized immediately for those presenting with vision loss, and also preventing further vision loss by treating it aggressively.
Jeff Bennett:
I’ve had the opportunity to both practice, to do research at the bench in this disorder as well as to move forward in participating and designing some of those clinical trials that you’re going to hear about today. Look forward to talking with all of you.
John Rose:
I’m John Rose from the University of Utah and I’m involved with Data Coordinating Center for all of the data that comes in from the find studies from the foundation. In addition, I’m a practicing neurologist and head of neuro immunology and virology division at the University of Utah. We have, in my lifetime had the perspective of going from understanding that the antibodies or some sort of a Y shaped molecule, to understanding advanced molecular biology of these pathogenic proteins and how the new tolerance initiatives and things of this sort, the new strategies for treatment that are rising, it’s just really phenomenal to see.
John Rose:
You’re living in an age of advanced science impacting major diseases. We’re seeing lots of good results in our clinic populations. And I’m sure all of the people on the stage here would say that there has been a significant revolution so far, but we have more to accomplish. Look forward to that.
May Han:
Good morning. My name is Dr. May Han and I’m a neurologist at Stanford University. I take care of patients with NMO and neuro inflammatory disorders. Outside of being a clinician, I also do research on neuro myelitis optica and other neuro inflammatory conditions. I’m very interested in the biomarkers and identifying molecules that can predict relapse in NMO. The other part of the equation that I’m involved in with the NMO care is I’m part of the CIRCLES study, as well as I’m very active in patient education, as well as having an NMO local family at Stanford, through the Guthy-Jackson supported Patient Day effort, as well as organizing NMO advocacy at Stanford. It’s wonderful to see new faces as well as some of the very familiar faces that I’ve seen at home. Look forward to having a productive day with you today. Thank you.
Maureen Neely:
Hi, my name is Maureen Neely and I started working in NMO with Ben Greenberg back in about 11 years ago. And then I’ve been with Dr. Levy for about almost eight years. I started mostly as a clinical nurse and have with Dr. Levy been more in the trenches with research and I’m currently working on my PhD where I’m looking into symptoms, particularly pain for patients with NMO.
Michael Levy:
I’m Michael Levy, and this is my eighth patient day. I’ve only missed one so far. I’m happy to be here. Thank you for inviting me again. And I’m at Johns Hopkins I’m a neurologist. I see only NMO patients on Fridays, and on Monday through Thursday, we’re in the lab. We’re developing animal models for NMO mostly in mice. And we now have two ways of curing mice with NMO. So, I think it’s just a matter of time before we get it into the clinic, and these are tolerization therapies that Dr. [inaudible 00:07:32] was talking about. So thank you again.
Moderator:
What we’d like to do is welcome anyone who’d like to have a question or comment and then get a response from one of the panelists. If you would, please limit yourself to one question, we can come back to you if you have more than one question, but we’d like to try to give everybody a chance. Okay, let’s start over here, please. No? Sorry where here. Thank you. Please.
Laura Frissell:
Good morning. My name is Laura Frissell. I was diagnosed with NMO, almost three years ago. I’m currently pregnant. I’m eight weeks. It wasn’t expected. I was on Rituxan and Mycophenolate in the past. However, Mycophenolate gave me an infection in my esophagus then they move it to Rituxan. I had two infusions and both times I had an allergic reaction. So right now, they only have me on [inaudible 00:08:41] and Lyrica but they’re trying wind me off because of the other baby. So my question is, do you have any safe treatments that I can be put on while I’m pregnant? And if there is a high risk of a worst relapse after I’ve giving birth?
Moderator:
Okay, starting off with a good question. Nancy, please.
Nancy Sicotte:
I’ll start. But I also defer to folks who take care of a lot of patients. I managed a patient who was pregnant with NMO and it was a planned process, and we were able to use Rituxan. That’s can be helpful because of the long acting effect of the B cell depletors. For an unexpected pregnancy, that’s another challenge. During pregnancy, steroids, of course, are considered to be safe. If you were to, hopefully not but if you had a relapse, for example, that could be a treatment. There is evidence that lower doses of Azathioprine are safe during pregnancy. So that’s another potential consideration especially since now you’re eight weeks and past the time when organs are forming. In terms of using B cell depletor, it sounds like Rituxan’s not an option for you because of allergies.
Nancy Sicotte:
There is another B cell the depletor called Ocrevus that we use in multiple sclerosis. It hasn’t really been used extensively in NMO patients, but it has a similar action. That’s not considered to be safe during pregnancy because it would deplete B cells in the baby as well. I think it’s definitely an area where we need more information. In terms of the relapse activity, we know in MS the relapses go down during pregnancy, there’s some evidence that that may not be the case with NMO and it does seem as though postpartum there is also a risk. So it’s almost as though there’s a double whammy of both increased risk during pregnancy and then in the postpartum period, so it definitely would require close follow up and close work with your neurologist. But I defer also to my colleagues if they have other experiences.
John Rose:
I’ve had two pregnancies and one patient recently. And so we looked at a lot of this literature and what Nancy has said is what we found quite a bit. In one, the first pregnancy the patient had to go off of her immunotherapy, which was CellCept, she shouldn’t have gotten pregnant on that drug. So fortunately, everything went well. And we just plan to give her Solu-Medrol treatment a few times during the pregnancy just two, and once after the pregnancy. And that went quite well actually. I don’t think you can really predict in a patient, is a pregnancy going to be associated with a relapse or not. Some people have also mentioned using IVIG as a possibility. We had that experience with Solu-Medrol in the first pregnancy.
John Rose:
In the second pregnancy, we had given half of the cycle of Rituximab before the pregnancy was detected, and before the second treatment can be given. And so we just monitored the B cell counts and we got through the whole pregnancy with a low B cell count in that particular case and didn’t have to administer Solu-Medrol again. But our high risk pregnancy clinic has always said that we could give Solu-Medrol during pregnancy. So, that may be the best consideration.
Moderator:
John, thanks a lot. We’re going to move to another question. Over here, please.
Eileen Whipple:
Thank you, good morning. I’m Eileen Whipple. I’ve been diagnosed 20 years. I just wanted to know what you guys anybody knows about NRF2 activation and NRF1 activation. And if you do know about it, what you’re doing to implement that in your research studies?
Moderator:
Michael, Jeff, John.
John Rose:
Well, we use this medication called Dimethyl Fumarate for multiple sclerosis patients. We’ve been studying that in mice recently to look at its overall properties in a progressive neurological model that occurs after a viral infection. And I think we’re seeing some very interesting properties, suggesting that there could be benefits beyond just with the immune mechanisms and perhaps providing some protection and repair. So we think that this is a very important system to be studying and looks very promising to us.
Eileen Whipple:
Thank you.
John Rose:
It could be applied to Neuromyelitis optica of course.
Moderator:
Michael, did you want to follow?
Michael Levy:
Yeah, the NRF2 system is thought to act by being an antioxidant, and neuroprotective in many different conditions. So people are considering it for NMO, but how exactly to stimulate it and how to reap the benefits of those antioxidant properties is not exactly clear. Maybe it would be on a preventive basis, or even during a relapse, so we don’t have those answers yet. But it’s something that we’re looking at in other fields to inform for us here in NMO. Yeah.
Eileen Whipple:
Excellent. Thank you.
Moderator:
Let’s take a question from the center.
Sandra Adda:
Hi, my name is Sandra Adda. I’ve been diagnosed 10 years now with NMO. About three years ago I started getting one infection after another and come to find out after a year and I think I’ve spoken to about this Dr. Levy. I was diagnosed with hypo… That’s a mouthful. Hypogammaglobulinemia. And for the first year, no one could figure it out. In fact, I was in the hospital with a 20,000 blood count and emergency surgery. And a year later, my MS specialist found out that it was caused by Rituxan. I’ve been stable on Rituxan for 10 years now, thank God. But I’ve now developed this additional diagnosis which I have to do IVIG along Rituxan but on sub-Q every two weeks. This is a two part question because someone who’s not here and that’s in our group. My question is for me, which I’ve asked my immunologist and neurologists, am I going to have to be on sub-Q IVIG for the rest of my life to replace my immunoglobulins my IgA and IgM never go up, but my IgG does go up because I’m on IVIG every two weeks.
Sandra Adda:
Part of the question is I only do one gram every six months, I’ve never done the two grams. For a friend of ours that’s in the group. She was doing two grams in her now she’s cut back to one. For me, I guess the way my neurologist is asking now I get my B cells checked every single month after the third month, but now he’s thinking about instead of doing Rituxan every six months for me, he may just do it based on if my B cells are going to elevate only because the Rituxan is killing my immunoglobulins and again, I’m on IVIG every other week. Am I going to have to be on this for the rest of my life? Will immunoglobulins ever replace on their own without the IVIG? I think that, my MS specialist only knew about the immunoglobulins and that needed to be checked. My IgGs never got checked seven and a half years before, this was only because I kept getting sick and they found this out.
Sandra Adda:
So, is that also a test that everybody should be getting along with their bloodwork, the IgGs just in case that this can happen. And again, will my immunoglobulins ever placed by themselves without high central treatment basically every other week? Thank you.
Moderator:
Jeff, could you handle that one please?
Jeff Bennett:
Sure. Sorry to hear that you’ve had this complication from the Rituximab therapy, but it’s something that you’re bringing up that’s important to know for everyone in the room who’s on Rituximab, very important for the physicians to know who take care of it. I can’t comment on what your physicians did or did not know about Rituximab but one of the reasons why it may not have been checked is that Rituximab is an antibody against CD20 which is present on the surface of B cells and is lost on the surface of those cells when they mature to antibody producing cells. And those antibody producing cells go to tissue sites, such as the bone marrow in particular, and, “live a long time pumping out antibodies” that serve as one of the protective mechanisms of your immune system.
Jeff Bennett:
What happens in those long live tissue cells was thought to be immaterial to the use of or Rituximab because they didn’t have that molecule on the surface and wouldn’t be depleted in patients treated with it. But they may not be as long lived as we think they are, they may need to be replaced at somewhat of a regular basis. And we’re now understanding that a significant fraction of patients with long term treatment with a B cell depleting agent such as maybe about as high as 20% may get into a hypo gamma globulin state, the lack of IgG. Unfortunately, our best way to immediately effect that is what you’re doing is to give you the antibody back again. Now unfortunately, that is just like any other medicine, it’s going to last a certain amount of time in your bloodstream. And then you’re going to have to give it again, just like if you take a pill once a day, you’re going to have to get this, based on the roughly two week half life of that IgG, that is five of those go away.
Jeff Bennett:
It’s all going to be gone from what we gave you, but it’s not addressing the primary problem. I watched my patients very closely for this, especially those that have been on for a number of infusions to either detect it early, or once I see it starting, I have to make a judgment and so does the patient is that watching it asymptomatically, certainly if someone’s having infections we treat it, but then deciding what to do is you’re questioning, what am I going to do to stop this from going on and on? And you’ve hit the nail on the head is that you really have to stop the depleting process and allow those cells to come back and take hold. With that comes the potential risk of having an attack. And we don’t have the actual marker to look at what it would be about the B cell population right now, that might imply that if you were to stop it, lower the dose significantly or increase the interval between infusions, what it would be to look for to say, hey, we’ve done it too much, you’re at risk now.
Jeff Bennett:
But I think switching to an alternative therapy, while you either stop that or significantly lower the dose, and I would consider stopping it for a while because often if you’ve been on for a number of years, it’s going to take you almost a year plus, to start to reconstitute your B cells, is going to be probably the best long term strategy to try to replete that IgG, get you of off the IVIG, which has positive effects. So you’re not treating yourself for the medicine that’s going to place you at additional risk, but it’s certainly going to be a regular complication for you. And it’s the only thing that’s going to allow those other letters in the alphabet suit the IgM, the IgAs to start to come back as well.
Sandra Adda:
Thank you for that response. But I think the question also was, for me I chose Rituxan as my drug of choice, even knowing it wasn’t FDA approved. This was 10 years ago and again, I’ve been stable on it for 10 years. I and my doctor were very conservative of only given me one gram thank God, because who knows what would have happened if I gotten one gram two weeks apart and doing two grams. I’ve always done one gram, I really can’t go off Rituxan, I don’t want to, because wouldn’t self set or [inaudible 00:21:56] it being immune suppressed drug that can do that to your IgG levels too, I would assume. However, so I guess what I’m saying is instead of doing it every six months should we do it based on… Because I can’t lower my dose of Rituxan, but maybe go eight months and based on my B cells, because I am doing the IVIG sub-Q every two weeks.
Jeff Bennett:
I mean, you could go to nothing for a year and watch the B cells.
Sandra Adda:
And just stay on IVIG?
Jeff Bennett:
Yes.
Sandra Adda:
Okay. Thank you.
Moderator:
Jeff. Thanks. We’re going to have a question here, please.
Sharon Ransom:
Hello. My name Sharon Ransom. And I first want to say that I was misdiagnosed for 25 years with MS. I’ve been on Rituxan for about the same amount of time, nine or 10 years. My neurologist at this point is concerned that with the length of time I’ve been on Rituxan that either I was getting the two doses every two weeks for about four or five years. She reduced it to one dose now every six months, but I’m still having reactions to the Rituxan even though she reduced the amount. My last visit with her, her suggestion began to be maybe only needed every nine months or once a year. This is a follow up question to the young lady that asked the question previously. Another drug that you or someone on the panel spoke about it began with Ocrevus or something like that.
Audience:
Ocelizumab.
Sharon Ransom:
Ocrelizumab, okay. That had been suggested if the Rituxan gives me problems. I wanted to know what you or someone thought about that. And if you have any data on people who have been Rituxan over five years. I was told that at first the thought was that five years would be the therapy for NMO and Rituxan.
Moderator:
May, could you?
Nancy Sicotte:
Michael did you say my name or someone else?
Moderator:
I was going to ask May, but please go ahead.
Nancy Sicotte:
I was just going to briefly say about the Ocrevus Ocrelizumab. So that’s a new drug that is very similar to Rituxan but more humanized, has less of the mouse component. So usually the infusion reactions are lower. I have an interesting case of a patient who developed Rituxan antibodies and did not deplete so we she kept getting Rituxan and then we check her B cells and they didn’t go down and then lo and behold, she has anti Rituxan antibodies, so we just got approval to try Ocrevus with our Ocrelizumab and I’m very curious to see if that works. One of the issues, of course, is insurance, because it’s not… there is no FDA indication for B cell depleted for any drug right now for NMO. So, some of the issue is getting the approval.
Nancy Sicotte:
I do think it’s a great question. And I’d love to hear the rest of the panel’s thoughts about the double dosing, because there does seem to be patients out in the community who are getting 1,000 every two weeks, every six months. So doing what we call the induction, but continuing to do that repeatedly. And as far as I know, there’s no evidence that that gives you an extra benefit, because the B cells are completely depleted if you just do the one 1,000 dose. And truthfully, if you did 500, you’d probably deplete B cells completely. Part of the question is how quickly they come back. And we do monitor that over time to make sure if somebody needs to be dosed more frequently, but I don’t think there’s any advantage to doing the two 1,000 doses continuously.
Nancy Sicotte:
I think maybe we will start moving to this model of monitoring B cell return, the issue within NMO though is that sometimes disease activity comes back just as the B cells are starting to reappear. So it can be very tricky in that regard, so I’d like to hear what the rest of the panel has to say about their experience.
May Han:
In follow up to that question, we have also had a number of patients who are on Rituximab for a period of time and B cell count of zero. And the question comes up how and when to redose them. In our institution, we’ve been following a B cell marker called CD27, together with a total B cell marker, CD19, as well. This is still very preliminary. By using that new marker, we are hoping that we’ll be able to dose the patients according to the cell count as opposed to dosing them every six months. As more information comes with the new biomarkers, we hope that we’ll be able to titrate the medication dosing according to the patient’s immune set status as opposed to a fixed dosing.
Ardith Courtney:
I just wanted to add to that, that we thought zero, zero. We did a study looking at patients using a lower dose in part because Rituxan wasn’t a covered drug, and some patients couldn’t get it. So we thought, why don’t we try to use a partial dose and see what happens. And we followed patients B cell counts and they would in fact go to zero, we lower doses, they would come back more quickly. The other issue for me is I used to watch these counts all the time and then dose patients on the medication based on what their counts were.
Ardith Courtney:
But one of the problems is the cell counts can come back very quickly. And then I’m fighting to get the medication, and in that period of time the patient’s going on and having a relapse with very low B cells but they have returned. It’s tricky, it’d be nice to find markers that helps us know number one when a relapse is coming. And if there’s anything else that help us figure out when that next dose is due, but obviously we’d like to use as little medication as possible, for many reasons. But I think that there could be some problems with that.
John Rose:
I think this points to the importance of the new monoclonal antibodies targeting other systems that may emerge in the next year or two years, widening the therapies.
Moderator:
One of the things that I hope we’re all understanding is that not all B cells and T cells are created equally. So one thing is how many of them there are. The other is, are there those that are autoreactive. If you have all B cells that are… You could have the highest number of B cells possible. If none are autoreactive, that’s fine. Or you can have low number of B cells, if many of them are autoreactive, that’s a problem. This is a point that I think leads us to the concept of personalized and precision medicine. That the whole field of medicine is moving toward, and one of the things that we can keep coming back to is, as Ardith pointing out, how to best treat each person, not just their disease. And that has to do with something called pharmacogenomics how the body handles that medicine might be different in one person than it is in another person.
Moderator:
Also, getting back to the point about pregnancy, how antibodies might move from the periphery of the mother into the protected environment of the fetus. All those things are really under rapid evolution right now scientifically, and it’s all under the file of personalized medicine. So very important points, let’s say ask a question over here, please.
Heather:
Okay. Hi, my name is Heather, I have a question about the Aquaporin-4 and MOG. It’s from the whole [inaudible 00:30:11] family pages on Facebook. So we’re curious. Quite a few patients started out as Aquaporin-4 positive with NMO IgG tests. So they were positive and then they went on treatment, whether it was Rituxan, or Rituximab. But now they reverted back to negative. What does that mean in terms… obviously, the treatments are working, something’s working for them. But a couple of patients, they’re coming back and they’re not sure. Their doctors are saying, “Well, maybe you’re not positive.” But we were always told from the beginning that if it was positive, once you’re positive, it doesn’t change. I’m just curious about has that ideal changed? Or did we miss something?
Moderator:
Michael, do you want to start off on that one?
Michael Levy:
In NMO with Aquaporin-4, I would say that one’s positive always positive. I don’t even bother rechecking patients unless there’s a question about their diagnosis. But once the diagnosis is made, the Aquaporin-4 antibody doesn’t really help that much more. But I think MOG might be different. We don’t know for sure, but sometimes, patients who are diagnosed with a MOG antibody with just one attack may never have another attack again. But they might and it may depend on whether the antibody persists. So, MOG and Aquaporin-4 might be different in that regard. We’ll have to… Maybe next year we’ll have the answer about the MOG antibody, but for now with Aquaporin-4 that rule definitely applies once positive, always positive.
Moderator:
Jeff.
Jeff Bennett:
Yeah, I’ll add a little clarification for one of the things that you mentioned was that someone said maybe, person was not really positive. When someone has a single test and a standard clinical event that is characteristic of this disease. And however it’s measured in an appropriate fashion, the antibody is high positive, it’s usually not repeated. But sometimes patients show up and they have an unusual neurologic symptom. Someone for some other reason tests them for Neuromyelitis optica and the antibody shows up at a borderline level. It may be retested with the idea that the test is a false positive. And that has to be done for many other different reasons. And they might be retested and it’s negative again right away and then they’re told really that maybe you really weren’t positive.
Jeff Bennett:
On the other hand, as mentioned, some patients with therapy do Sero-revert. And the question that’s very important in that is, is that telling us something? We have done many studies now looking at the level of antibody in patients, and whether that’s related to risk of disease activity that is new attacks or the severity of those attacks, and we haven’t really found that link. But when someone reverts, that could mean that something substantially different has happened in the disease. And why we can’t say for sure, because as you’ve heard about tolerizing your immune system as an ultimate goal of cure, that is to make you not reactive anymore. As we’ve mentioned, those cells may not live forever.
Jeff Bennett:
So we expect that your titer of antibody should either go down substantially or disappear if you’re tolerized. That may be the effect that we’ve done something substantial. But the problem is, there are that fraction of patients about 25% who qualify for disease and do not have antibody that we don’t know whether we’ve shifted your category, or done something substantial to prove it. So that’s why other markers are going to be necessary to say maybe that’s the first tip off of you can come off therapy.
Moderator:
Maureen, maybe I could just ask you to follow up on pain with respect to antibody status. Are you finding any differences thus far that you can comment on?
Maureen Neely:
Well, I don’t think that that’s been looked at broadly, but I’ve never heard of pain being a marker of antibody status. I don’t know of anything about that.
Moderator:
Okay. Gabriela.
Gabriela Romano:
Thank you. I’m Gabriela Romano. And my question is, if this is a rare disease, and we’re all excited about the results of the clinical trials, let’s say one of them comes through and is FDA approved. In your experience as doctors, will you automatically change everyone’s therapy to the new FDA approved drug or will you keep people on the drugs they’re on if they’re being effective? And do you have any idea what will happen with insurance? Thank you.
Moderator:
Ardith would you like to try that one?
Ardith Courtney:
A lot of reaction there. So no, I wouldn’t automatically switch somebody over. I think that ultimate goal of having a very effective and very safe medication may be a little further off. If it were the case that we had a very effective medication and it was very safe, I may look at that medication different. But if we’re looking at the same safety profile for medications I’ve been using that have been effective in a patient. I don’t see any reason to really change. Unfortunately, most of us don’t have 10s of thousands of dollars to spend on our medications and insurance comes into play sometimes. I think early we’re going to have a lot more on laterality and as physicians we’re able to prescribe for patients because we realize that not one medication is a fit all for every patient. There may be very good reasons for us to be able to say to an insurance company, this is a medication, It’s been effective and the patient’s been on and I think it’s the right safety profile for them.
Ardith Courtney:
But as more drugs come into the market and they’re FDA approved, then the insurance companies then are able to make deals with those companies. And it may be a little bit more complicated, but I think we’ll have a little bit of a honeymoon period where we will have that laterality and then always with a fight sometimes we’re able to get the right medication for that patient, whether it’s FDA approved or not.
Moderator:
Ardith thank you. Let’s take a question over here, please.
Andrea Mitchell:
Hello, my name is Andrea Mitchell. And I’m back. I’m just back to ask if there’s any updates at all for antibody MOG. I heard a lot about tolerization with Aquaporin-4 and I’m wondering if anyone’s doing research with tolerization and the antibody MOG. I’m hoping the MOG hasn’t got lost. If anyone could please. If you have any updates, please share them.
Moderator:
I could update you, Andrea. In a meeting in London that took place in January of this year. The major focus was on the differences between Anti Aquaporin-4 positive disease, and anti MOG positive disease. The group from the UK headed from Oxford and that large number of researchers looking at that problem does plan to focus on telogenesis against MOG. It’s a tandem approach with a group focused on tolerizing Aquaporin-4, another group focused on tolerizing MOG. So there’s a dual approach to this right now. So it’s a great question. There’s a lot of people focusing on MOG. Thanks for that question.
Moderator:
We have a question in the back here. Sorry.
Tanisha Owens:
Good morning panel. My name is Tanisha Owens from New Jersey. I was actually looking forward to giving the question to Dr. Levy since I was a brief patient of his at John Hopkins last year. I basically had been diagnosed with MS for 10 years and been relatively stable on treatment until I was diagnosed with NMO last July, and it hit me pretty hard. I was on Rituxan only at two doses, I kept relapsing so to speak, so I was receiving plasmapheresis PLEX. And what I found was that the PLEX significantly helped me. And every time I was getting into three times a week, my symptoms improve dramatically, as well as my deficits, you see, I’m standing here walking and seeing you today. I’m now seeing a doctor at NYU who’s amazing, but he [inaudible 00:39:11].
Tanisha Owens:
I constantly battle with him back and forth because although I am doing okay, I just wondered specifically, what are your thoughts about the plasmapheresis as far as not so much… Are you looking at plasmapheresis as possible maintenance therapy for people such as myself, because I do tend to… The antibodies tend to keep coming back on such a dramatic level. And he on other hand doesn’t believe in it. And we do have a family member who does get maintenance plasmapheresis which tends to help. I’m just wondering with your knowledge, what are your thoughts on the PLEX in patients as a maintenance therapy so to speak?
Moderator:
May, do you want to start?
May Han:
That’s a very important and a good question. So plasmapheresis maintenance is not for every patient. But then we have also had a handful of patients who had several relapses on Rituximab or other biologic therapies. Rituximab maintenance therapy is the only thing that works for them. For those patients who have done plasmapheresis on scheduled intervals, and that has worked out for them.
Audience:
I have a question.
Moderator:
Oh, sure.
Audience:
Very exciting about just the research that you’re doing in trying to prevent looking at antibodies, looking at the B cell counts to be able to prevent, knowing when a relapse will occur. My question is, what about in patients where there’s a relapse and you’re at zero? Is that being looked at all as well or are all of those things being looked at together? And what do you do in that circumstance? Or do you not experience that?
Michael Levy:
We looked at our Rituximab failures and found that about 10% of cases were in the context of a zero B cell count. These are folks who got their treatment on time and they did everything right. But they had a relapse, and we checked their B cell count at the time of the attack, and it was zero. And you’re thinking yourself-
Audience:
Yeah. And it’s confirmed on MRI still and it’s zero.
Michael Levy:
Yeah, there’s still an attack. It’s very evident attack, so what happened there?
Audience:
That was my question.
Michael Levy:
Well, maybe there are other B cells that are involved. Rituximab only depletes about two to 3% of all your B cells, only the ones in the bloodstream and a few lymph nodes. The rest of your B cells are still there. Maybe they’re taking part, maybe. Or maybe it’s it’s a disease process that’s going around the B cells, you have lots of other immune cells that are involved in NMO, and maybe it found a way to do it without the B cells.
Audience:
Could tolerization, maybe also address this issue as well?
Michael Levy:
Yeah, I think tolerization is more of a whole immune cell approach to try to really re educate the entire immune system rather than targeting just one area. And I think it has more potential to do just that.
Audience:
Okay. Thank you.
Moderator:
We have about 10 more minutes or so with this session. So, if we could make the questions brief, and hopefully the responses brief, we can get a few more in, please.
Adeli:
Good morning. My name is Adeli. I’m from Massachusetts first time here. My question is more for muscle spasticity. I can’t even say it right. I’m a mother of two, I have a two year old so I got to run around a lot. I just need I guess something other than baclofen because it doesn’t really work for me to basically be a mom and run around.
Moderator:
Nancy.
Nancy Sicotte:
That’s a very challenging symptom to deal with, especially when you’ve got little ones that you’re running around chasing. There are other medications for spasticity. Another one is Tizanidine or Zanaflex but in my experience that can make you really sleepy, especially when you first take it. We’ve had some success with another medication called Dantrolene or Dantrium. That requires careful monitoring of your liver enzymes, but that’s not as sedating. And so that’s another option. And then if you have very focal areas where you’re having spasticity, we sometimes use Botox. So rather than just relax the muscles in your face, like they do a lot here in Los Angeles, this would be there to really relax if you had very specific muscles. You have to do that carefully also, because it can make you weaker and a little bit harder to walk. The other thing is non medicinal things like stretching, yoga, those sorts of things can also be really helpful in dealing with some of the spasticity. It’s a multi-focal approach.
Maureen Neely:
If I can just add. To add to what she just said, we have a lot of patients respond differently to different treatments. It’s really across the board. But in addition to some of the things she said, Aqua Therapy, that’s very helpful for spastic muscles. And so, getting tied in with a physical therapist who knows a lot about spinal cord rehabilitation is always beneficial. As well as massage therapy, it can go either way. Some people say that it worsens their symptoms. Others say that it’s a real lifesaver. And so there is a lot of trial and error involved in terms of both the medications and non medicinal treatments. And so it takes a lot of patience, and it takes a good collaboration with your medical team in order to come up with the things that help you. But we also know things like sleep are affected. Both affect muscle spasticity and muscle spasticity worsens sleep, so really paying attention to some of those other co occurring symptoms can help out as well.
Moderator:
Maureen thank you. We’ll move to the next question, please.
Jennifer Alfonso:
Good morning. I’m Jennifer Alfonso, and I want to follow up on Andrea’s question about MOG. I know we were told that a lot of people are working in research in MOG. I specifically would like to know what’s being looked at in MOG. Also wants to know if you had a preference in terms of preventative treatment that you’re doing for MOG from the one you think is most effective to least effective, and if there are any clinical trials right now in the pipeline for MOG.
Moderator:
I can start on what’s being done in terms of some of the priority research. For example, large data banks and bio banks of Sero that had been seen originally as Sero-Negative are being screened for MOG. In the last couple of months, there has now an approved assay for MOG antibody, there has not been one until now. In effect, it’s now a formal test that can be done. A lot of times, and we can ask the panel that a lot of times in individuals who are tested as Sero-Negative but have all the symptoms of NMO, if they’re tested for Aquaporin-4 and it’s negative, now the tests can be done on MOG. Without going into all the details of the epidemiology and molecular biology of MOG, because as you know, MOG antibody is a response to a cell that’s different from the astrocyte, so Aquaporin-4 is to the astrocyte, as MOG is to the oligodendrocyte.
Moderator:
Different cells, different proteins, the immunology is different. There’s a lot of research around that. We could talk more about that. Jeff, for example, do you want to talk about perhaps treating MOG positive versus Aquaporin-4 positive disease differently?
Jeff Bennett:
Well, I think one of the most important studies that are coming out right now are clinical studies to help us differentiate what is MOG disease and what is Aquaporin-4 NMO. And because many different disorders can have clinical overlapping symptoms, many people with MOG disease will not have criteria clinically to qualify for the diagnosis of Neuromyelitis Optica and never will. There’s only probably a small fraction of those patients who will, and then understanding what they best respond to and how best to treat them as the next level of clinical research. Right now we understand the pathology from Nervous System tissue that’s affected is different between the two disorders. Again, encouraging us that they are likely clinical mimics of each other that demand special attention and differentiation because the most important thing we know is, if you’re MOG positive, you’re not Aquaporin-4 positive, and vice versa.
Jeff Bennett:
So then identifying someone who has an attack that may clinically look like NMO and is MOG may demand different treatment than someone who is Aquaporin-4 positive. And one of those things that maybe’s coming forward is, while both conditions don’t respond well to standard MS therapies, MOG based disease may respond quite differently or at least at less efficient levels to B cell depletion than NMO Aquaporin-4 patients do.
Moderator:
Jeff.
John Rose:
There has been a wealth of studies on MOG as an antigen for inflammatory demyelinating diseases of the central nervous system in mice, and we need to maybe revisit what all those studies showed, in both a cellular component and an antibody component may be important in that system.
Jeff Bennett:
I think what Dr. Rose is bringing up is that we’ve been studying MOG for a long time, it’s been an antibody in search of a disease for a long time. And researchers have labeled it as a model of MS for a long time. And I think, basically, it’s time to step back and go, oops, maybe we’re modeling something else for a very long time.
John Rose:
There’s going to be some crow to be eaten in this field, I think that…
Moderator:
Let’s move-
Nancy Sicotte:
But interestingly, there are many, not many, but there are certainly things that cure EAE, which is this MOG animal model that don’t work in MS. And I’m thinking of TNFalpha blockade, so there are medications on the market called embro, and other things for rheumatoid arthritis. If you give it to somebody with MS, it makes their MS worse, but if you use the animal model it actually cures it. The problem is I don’t think anyone’s brave enough to give it to a patient without some other information because it does make MS worse and so there’s a possibility it could make MOG worse. But it’s an intriguing and it might be a proof of principle that that EAE model would turn out to be a good predictor of treatment response. And then the only other thing I would add, I have one patient who’s anti MOG who has recurrent optic neuritis. And I don’t know if Jeff if you have some other folks like this, but we’ve tried everything with her, but she’s completely steroid responsive.
Nancy Sicotte:
As soon as her prednisone level goes below 10 a day she relapses and we’ve depleted her B cells. We’ve given her Azathioprine, she’s ALC low, but it’s a very steroid responsive, so I don’t know if you have experience with them.
Jeff Bennett:
No, MOG could be uniquely steroid responsive in many patients. And trying to educate other ophthalmologists, neuro-ophthalmologists about the high risk of MOG disease in someone who has recurrent optic neuritis, but again, it’s not all of them. I see too many patients with recurrent optic neuritis and of course, the first few that I checked with that for MOG were positive. And I patted myself on the back and thought how smart I was until the next 10 that I did that didn’t have it. Then I think we learned that there are many in that category that don’t. But we’re starting to learn that so many of these disorders have overlapping clinical symptoms. And what’s going to clue us in on the best therapy is all these new markers, some of which Michael mentioned before.
Moderator:
Moving to the next question, please. We’ve got two brief questions, please.
Samantha:
Hi, my name is Samantha and I was diagnosed in February of 2016 with NMO’s transverse myelitis. My question was when it comes to relapses. I have two hospitals that I live in between, they’re not my primary hospital. Every time I fear that I’m having a relapse, because I’m not sure if it’s a relapse or pseudo relapse, I’ve gone to the hospital maybe several times. And so my question primarily is, when I wind up in one of those hospitals, how do I get the importance of trying to get across to them? “Look, I think I’m having a relapse, help me.” Opposed to them saying, “Yeah, okay. Just wait over here, because we don’t know what NMO is, so we’ll get to you when we get to you.” With respect to that, I’ve had to be transferred to my primary hospital a couple of times, because I felt like they have my file and they could help me more.
Samantha:
When I wind up in a situation like that, what is the best way to handle that so that I can get some assistance. Although they weren’t actual relapses thank God because I waited like six, seven hours to be transferred, and then another four or five hours to be seen. So without acting crazy what’s the best way that somebody can handle that?
Ardith Courtney:
I think the best answer to that is that have your doctor’s personal telephone number and call them at two o’clock in the morning just easy. I really honestly don’t think that any emergency department is the best place. It is important to have a physician who understands what it is that you have, and is your advocate basically. Because it’s a lot easier for a physician to talk to another physician, you come in and say, “You know, I’m having new numbness and tingling in my legs or maybe I’m having a little bit of vision problems.” And you are able to have that physician or somebody who knows you talk to that other person because it is important that you’re treated and you’re not sent away or not looked at basically.
Ardith Courtney:
I just think it’s having a good team of doctors or people that know you who can interface with them if at all possible. The other thing is that you probably know more about Neuromyelitis Optica than a lot of physicians. And so it’s sometimes it’s helpful to have a copy of your consult letter or laboratory or both with that information on there, so that when it’s summarized usually when we do the initial consult and you get through diagnosis, where you usually putting in there the diagnostic data that allowed us to make that diagnosis, and what our thoughts on what we think needs to happen. And if you have that piece of paper for some reason, that gives you more credibility. It shouldn’t be that way. But sometimes this are busy people who just have never heard of Neuromyelitis Optica before and they truly don’t understand.
Ardith Courtney:
Having something in writing from your physician is helpful. And then I think also been in contact with them during the day, if at all possible, even if you’re thinking something might be going on that you’ve made a phone call maybe a couple days beforehand. And that way at least they have a heads up that something’s going on with you.
Maureen Neely:
To add to Dr. Courtney. I’ll also say I don’t know how much it would delay you to go to your primary hospital rather than your local hospital. But when you think of how much it delays you to go to your local hospital, and when you take into consideration maybe the severity of your symptoms, if they’re not so severe, it might be worth taking that extra hour or whatever to get to your primary hospital where you have a team who is so aware of your situation and your history with NMO.
Moderator:
I would just want to remind everybody that there are going to be three breakout sections later this afternoon on, ask the docs, and I suspect that’s going to be pretty packed. We always try to get to as many questions as possible. We’re going to end this session with one last question in the back, please.
Audience:
I have a general question I think apply for everybody. I’ve been reading that any autoimmune is triggered by a first infection, chronic infection and then on top of it a certain genetic disposition, like certain HLA genotype. What do you think of that? If you have some research on that? And thank you.
Moderator:
Michael, do you want to start on that one?
Michael Levy:
Yeah, I think it’s exactly like you say, I think there’s a genetic predisposition, we don’t know what it is. But a lot of my patients have autoimmune disease in the family like lupus and psoriasis. And that’s the genetic background that encounters whatever infection it is, we don’t know it could be maybe something in the gut, maybe an infection you didn’t even know you had because it was so mild. But whatever it was, it’s that combination of that environmental exposure and the genetic response to it that then turns on the NMO disease. And I think it’s exactly like you say. But there are some people who have no autoimmune disease in the family. And there are some people who say they’ve never had an infection. We don’t know exactly what it is. But even in mice, when we model it in mice, there’s definitely a genetic background, and an environmental component that contribute.
Moderator:
We would like to think of it as a combination lock with the tumblers if they all fall into place. But the funny thing is that the tumblers are not the same for every person. Okay. Thank you all very much for your questions. We really appreciate it. As I said, there’s going to be more opportunities to ask the docs this afternoon. We’re going to take a break now. A question in the back here, sorry. Please.
Tanisha Owens:
Good morning panel. My name is Tanisha Owens from New Jersey. I was actually looking forward to giving the question to Dr. Levy since I was a brief patient of his at John Hopkins last year. I basically had been diagnosed with MS for 10 years and been relatively stable on treatment until I was diagnosed with NMO last July, and it hit me pretty hard. I was on Rituxan only at two doses, I kept relapsing so to speak, so I was receiving plasmapheresis PLEX. And what I found was that the PLEX significantly helped me. And every time I was getting into three times a week, my symptoms improve dramatically, as well as my deficits, you see, I’m standing here walking and seeing you today. I’m now seeing a doctor at NYU who’s amazing, but he [inaudible 00:58:56].
Tanisha Owens:
I constantly battle with him back and forth because although I am doing okay, I just wondered specifically, what are your thoughts about the plasmapheresis as far as not so much… Are you looking at plasmapheresis as possible maintenance therapy for people such as myself, because I do tend to… The antibodies tend to keep coming back on such a dramatic level. And he on other hand doesn’t believe in it. And we do have a family member who does get maintenance plasmapheresis which tends to help. I’m just wondering with your knowledge, what are your thoughts on the PLEX in patients as a maintenance therapy so to speak?
Moderator:
May, do you want to start?
May Han:
That’s a very important and a good question. So plasmapheresis maintenance is not for every patient. But then we have also had a handful of patients who had several relapses on Rituximab or other biologic therapies. Rituximab maintenance therapy is the only thing that works for them. For those patients who have done plasmapheresis on scheduled intervals, and that has worked out for them.
Audience:
I have a question.
Moderator:
Oh, sure.
Audience:
Very exciting about just the research that you’re doing in trying to prevent looking at antibodies, looking at the B cell counts to be able to prevent, knowing when a relapse will occur. My question is, what about in patients where there’s a relapse and you’re at zero? Is that being looked at all as well or are all of those things being looked at together? And what do you do in that circumstance? Or do you not experience that?
Michael Levy:
We looked at our Rituximab failures and found that about 10% of cases were in the context of a zero B cell count. These are folks who got their treatment on time and they did everything right. But they had a relapse, and we checked their B cell count at the time of the attack, and it was zero. And you’re thinking yourself-
Audience:
Yeah. And it’s confirmed on MRI still and it’s zero.
Michael Levy:
Yeah, there’s still an attack. It’s very evident attack, so what happened there?
Audience:
That was my question.
Michael Levy:
Well, maybe there are other B cells that are involved. Rituximab only depletes about two to 3% of all your B cells, only the ones in the bloodstream and a few lymph nodes. The rest of your B cells are still there. Maybe they’re taking part, maybe. Or maybe it’s a disease process that’s going around the B cells, you have lots of other immune cells that are involved in NMO, and maybe it found a way to do it without the B cells.
Audience:
Could tolerization, maybe also address this issue as well?
Michael Levy:
Yeah, I think tolerization is more of a whole immune cell approach to try to really re educate the entire immune system rather than targeting just one area. And I think it has more potential to do just that.
Audience:
Okay. Thank you.
Moderator:
We have about 10 more minutes or so with this session. So, if we could make the questions brief, and hopefully the responses brief, we can get a few more in, please.
Adeli:
Good morning. My name is Adeli. I’m from Massachusetts first time here. My question is more for muscle spasticity. I can’t even say it right. I’m a mother of two, I have a two year old so I got to run around a lot. I just need I guess something other than baclofen because it doesn’t really work for me to basically be a mom and run around.
Moderator:
Nancy.
Nancy Sicotte:
That’s a very challenging symptom to deal with, especially when you’ve got little ones that you’re running around chasing. There are other medications for spasticity. Another one is Tizanidine or Zanaflex but in my experience that can make you really sleepy, especially when you first take it. We’ve had some success with another medication called Dantrolene or Dantrium. That requires careful monitoring of your liver enzymes, but that’s not as sedating. And so that’s another option. And then if you have very focal areas where you’re having spasticity, we sometimes use Botox. So rather than just relax the muscles in your face, like they do a lot here in Los Angeles, this would be there to really relax if you had very specific muscles. You have to do that carefully also, because it can make you weaker and a little bit harder to walk. The other thing is non medicinal things like stretching, yoga, those sorts of things can also be really helpful in dealing with some of the spasticity. It’s a multi-focal approach.
Maureen Neely:
If I can just add. To add to what she just said, we have a lot of patients respond differently to different treatments. It’s really across the board. But in addition to some of the things she said, Aqua Therapy, that’s very helpful for spastic muscles. And so, getting tied in with a physical therapist who knows a lot about spinal cord rehabilitation is always beneficial. As well as massage therapy, it can go either way. Some people say that it worsens their symptoms. Others say that it’s a real lifesaver. And so there is a lot of trial and error involved in terms of both the medications and non medicinal treatments. And so it takes a lot of patience, and it takes a good collaboration with your medical team in order to come up with the things that help you. But we also know things like sleep are affected. Both affect muscle spasticity and muscle spasticity worsens sleep, so really paying attention to some of those other co occurring symptoms can help out as well.
Moderator:
Maureen thank you. We’ll move to the next question, please.
Jennifer Alfonso:
Good morning. I’m Jennifer Alfonso, and I want to follow up on Andrea’s question about MOG. I know we were told that a lot of people are working in research in MOG. I specifically would like to know what’s being looked at in MOG. Also wants to know if you had a preference in terms of preventative treatment that you’re doing for MOG from the one you think is most effective to least effective, and if there are any clinical trials right now in the pipeline for MOG.
Moderator:
I can start on what’s being done in terms of some of the priority research. For example, large data banks and bio banks of Sero that had been seen originally as Sero-Negative are being screened for MOG. In the last couple of months, there has now an approved assay for MOG antibody, there has not been one until now. In effect, it’s now a formal test that can be done. A lot of times, and we can ask the panel that a lot of times in individuals who are tested as Sero-Negative but have all the symptoms of NMO, if they’re tested for Aquaporin-4 and it’s negative, now the tests can be done on MOG. Without going into all the details of the epidemiology and molecular biology of MOG, because as you know, MOG antibody is a response to a cell that’s different from the astrocyte, so Aquaporin-4 is to the astrocyte, as MOG is to the oligodendrocyte.
Moderator:
Different cells, different proteins, the immunology is different. There’s a lot of research around that. We could talk more about that. Jeff, for example, do you want to talk about perhaps treating MOG positive versus Aquaporin-4 positive disease differently?
Jeff Bennett:
Well, I think one of the most important studies that are coming out right now are clinical studies to help us differentiate what is MOG disease and what is Aquaporin-4 NMO. And because many different disorders can have clinical overlapping symptoms, many people with MOG disease will not have criteria clinically to qualify for the diagnosis of Neuromyelitis Optica and never will. There’s only probably a small fraction of those patients who will, and then understanding what they best respond to and how best to treat them as the next level of clinical research. Right now we understand the pathology from Nervous System tissue that’s affected is different between the two disorders. Again, encouraging us that they are likely clinical mimics of each other that demand special attention and differentiation because the most important thing we know is, if you’re MOG positive, you’re not Aquaporin-4 positive, and vice versa.
Jeff Bennett:
So then identifying someone who has an attack that may clinically look like NMO and is MOG may demand different treatment than someone who is Aquaporin-4 positive. And one of those things that maybe’s coming forward is, while both conditions don’t respond well to standard MS therapies, MOG based disease may respond quite differently or at least at less efficient levels to B cell depletion than NMO Aquaporin-4 patients do.
Moderator:
Jeff.
John Rose:
There has been a wealth of studies on MOG as an antigen for inflammatory demyelinating diseases of the central nervous system in mice, and we need to maybe revisit what all those studies showed, in both a cellular component and an antibody component may be important in that system.
Jeff Bennett:
I think what Dr. Rose is bringing up is that we’ve been studying MOG for a long time, it’s been an antibody in search of a disease for a long time. And researchers have labeled it as a model of MS for a long time. And I think, basically, it’s time to step back and go, oops, maybe we’re modeling something else for a very long time.
John Rose:
There’s going to be some crow to be eaten in this field, I think that…
Moderator:
Let’s move-
Nancy Sicotte:
But interestingly, there are many, not many, but there are certainly things that cure EAE, which is this MOG animal model that don’t work in MS. And I’m thinking of TNFalpha blockade, so there are medications on the market called embro, and other things for rheumatoid arthritis. If you give it to somebody with MS, it makes their MS worse, but if you use the animal model it actually cures it. The problem is I don’t think anyone’s brave enough to give it to a patient without some other information because it does make MS worse and so there’s a possibility it could make MOG worse. But it’s an intriguing and it might be a proof of principle that, that EAE model would turn out to be a good predictor of treatment response. And then the only other thing I would add, I have one patient who’s anti MOG who has recurrent optic neuritis. And I don’t know if Jeff if you have some other folks like this, but we’ve tried everything with her, but she’s completely steroid responsive.
Nancy Sicotte:
As soon as her prednisone level goes below 10 a day she relapses and we’ve depleted her B cells. We’ve given her Azathioprine, she’s ALC low, but it’s a very steroid responsive, so I don’t know if you have experience with them.
Jeff Bennett:
No, MOG could be uniquely steroid responsive in many patients. And trying to educate other ophthalmologists, neuro-ophthalmologists about the high risk of MOG disease in someone who has recurrent optic neuritis, but again, it’s not all of them. I see too many patients with recurrent optic neuritis and of course, the first few that I checked with that for MOG were positive. And I patted myself on the back and thought how smart I was until the next 10 that I did that didn’t have it. Then I think we learned that there are many in that category that don’t. But we’re starting to learn that so many of these disorders have overlapping clinical symptoms. And what’s going to clue us in on the best therapy is all these new markers, some of which Michael mentioned before.
Moderator:
Moving to the next question, please. We’ve got two brief questions, please.
Samantha:
Hi, my name is Samantha and I was diagnosed in February of 2016 with NMO’s transverse myelitis. My question was when it comes to relapses. I have two hospitals that I live in between, they’re not my primary hospital. Every time I fear that I’m having a relapse, because I’m not sure if it’s a relapse or pseudo relapse, I’ve gone to the hospital maybe several times. And so my question primarily is, when I wind up in one of those hospitals, how do I get the importance of trying to get across to them? “Look, I think I’m having a relapse, help me.” Opposed to them saying, “Yeah, okay. Just wait over here, because we don’t know what NMO is, so we’ll get to you when we get to you.” With respect to that, I’ve had to be transferred to my primary hospital a couple of times, because I felt like they have my file and they could help me more.
Samantha:
When I wind up in a situation like that, what is the best way to handle that so that I can get some assistance. Although they weren’t actual relapses thank God because I waited like six, seven hours to be transferred, and then another four or five hours to be seen. So, without acting crazy what’s the best way that somebody can handle that?
Ardith Courtney:
I think the best answer to that is that have your doctor’s personal telephone number and call them at two o’clock in the morning, just easy. I really honestly don’t think that any emergency department is the best place. It is important to have a physician who understands what it is that you have, and is your advocate basically. Because it’s a lot easier for a physician to talk to another physician, you come in and say, “You know, I’m having new numbness and tingling in my legs or maybe I’m having a little bit of vision problems.” And you are able to have that physician or somebody who knows you talk to that other person because it is important that you’re treated and you’re not sent away or not looked at basically.
Ardith Courtney:
I just think it’s having a good team of doctors or people that know you who can interface with them if at all possible. The other thing is that you probably know more about Neuromyelitis Optica than a lot of physicians. And so it’s sometimes it’s helpful to have a copy of your consult letter or laboratory or both with that information on there, so that when it’s summarized usually when we do the initial consult and you get through diagnosis, where you usually putting in there the diagnostic data that allowed us to make that diagnosis, and what our thoughts on what we think needs to happen. And if you have that piece of paper for some reason, that gives you more credibility. It shouldn’t be that way. But sometimes this are busy people who just have never heard of Neuromyelitis Optica before and they truly don’t understand.
Ardith Courtney:
Having something in writing from your physician is helpful. And then I think also been in contact with them during the day, if at all possible, even if you’re thinking something might be going on that you’ve made a phone call maybe a couple days beforehand. And that way at least they have a heads up that something’s going on with you.
Maureen Neely:
To add to Dr. Courtney. I’ll also say I don’t know how much it would delay you to go to your primary hospital rather than your local hospital. But when you think of how much it delays you to go to your local hospital, and when you take into consideration maybe the severity of your symptoms, if they’re not so severe, it might be worth taking that extra hour or whatever to get to your primary hospital where you have a team who is so aware of your situation and your history with NMO.
Moderator:
I would just want to remind everybody that there are going to be three breakout sections later this afternoon on, ask the docs, and I suspect that’s going to be pretty packed. We always try to get to as many questions as possible. We’re going to end this session with one last question in the back, please.
Audience:
I have a general question I think apply for everybody. I’ve been reading that any autoimmune is triggered by a first infection, chronic infection and then on top of it a certain genetic disposition, like certain HLA genotype. What do you think of that? If you have some research on that? And thank you.
Moderator:
Michael, do you want to start on that one?
Michael Levy:
Yeah, I think it’s exactly like you say, I think there’s a genetic predisposition, we don’t know what it is. But a lot of my patients have autoimmune disease in the family like lupus and psoriasis. And that’s the genetic background that encounters whatever infection it is, we don’t know it could be maybe something in the gut, maybe an infection you didn’t even know you had because it was so mild. But whatever it was, it’s that combination of that environmental exposure and the genetic response to it that then turns on the NMO disease. And I think it’s exactly like you say. But there are some people who have no autoimmune disease in the family. And there are some people who say they’ve never had an infection. We don’t know exactly what it is. But even in mice, when we model it in mice, there’s definitely a genetic background, and an environmental component that contribute.
Moderator:
We would like to think of it as a combination lock with the tumblers if they all fall into place. But the funny thing is that the tumblers are not the same for every person. Okay. Thank you all very much for your questions. We really appreciate it. As I said, there’s going to be more opportunities to ask the docs this afternoon.
