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Emerging Therapies Teleconference with Dr. Aaron Boster (Transcript)

Kasey Minnis: Good evening everyone and thank you for joining us. My name is Kasey Minnis and I’m with the Multiple Sclerosis Foundation and the Chair Person of the Awareness Committee. I’d like to thank you all for participating in this National MS Education and Awareness month special event. We are very pleased to be joined this evening by Aaron Boster, M.D. who is the Assistant Clinical Professor of Neurology at Ohio State University College of Medicine, as well as the Director of the Ohio State University’s MS Clinic, the OSU Clinical Trials Program, and the Infusion Center.

A board certified neurologist, Dr. Boster completed his two-year fellowship in clinical neuroimmunology in MS at Wayne State University in Detroit.  He’s conducted research in the use of intense immunosuppression in MS, into the effects of ethnicity and pediatric MS, and clarifying MS diagnostic criteria. Tonight he is going to be speaking on the topic of emerging therapies. Following his presentation, we‘ll have a Q and A session where you will have an opportunity to ask your questions to Dr. Boster.  So please join me in welcoming Dr. Aaron Boster.

Dr. Boster: Hello everyone.  Thank you, Kasey for those kind words.  I’d like to thank the MS Foundation for giving me the opportunity for speaking to everyone tonight, I don’t know about you guys, but on this end I feel like, ah, it’s a fire side shot on the radio which is a little odd, but it’s a lot of fun. I hope we have a nice discussion today.  A couple of things that the bio left out is that I made a decision to become an MS doctor at age 12.  My uncle was diagnosed with MS and progressed in his disease process long before drugs were available. He’s still alive and ironically he lives about 2 miles from my clinic. He’s pretty bad off and he never had the opportunity that hopefully many of you listening tonight have had in MS medicines.

The first MS medication was Betaseron, you’ll probably remember thinking back to 1993. I’m very proud that the 7th FDA approved medicine, Fingolimod was FDA approved just September of last year.  At our clinical trials program at Ohio State, we’re studying no less than ten other drugs and internationally there’s about 120 drugs coming down the pipeline. As twisted as this sounds, if you’re going to have to have MS this is the right time to have it. There’s a tremendous effort being made at working diligently to slow down your disease process and I’m really proud to be participating in that. I’m also excited that I get to talk to you tonight. 

I think if we’re going to think about MS let’s start at the beginning and talk about what MS really is.  To understand multiple sclerosis, I feel that we have to start with the immune system.  The immune system is made up of a bunch of white blood cells. These cells come out of your bone marrow inside the bones, they go to school up in your neck, and simply learn one rule. The only class they take is to identify self vs. non-self, and in actuality if they don’t pass that class the white blood cells are killed. So everyone that graduates should understand very clearly that when they identify a cell that is yours vs. one that belongs to a virus, bacteria, or whatever the case may be.  Now, once they graduate they are literally given weapons. They are sent out into the bloodstream and they do what soldiers do - they survey, they go around, they check everyone out. If they see any one of your own cells they smile and wave. If they see a foreign object, if they see a virus, a parasite, a bacteria; well they call their friends over and they beat the snot out of it and they lay waste to the virus.  More importantly, they make a memory of that virus. So where was the virus that revisits your body? Because your immune system has literally made an army that’s been waiting around for that virus to return, it lays waste to it again and that’s why we don’t get chicken pox two times. The second time we see the virus, not a big deal, we’re ready.

Now, just like, uh to continue my soldier analogy, when you’re on sentry duty you’re not suppose to shoot your buddy - no friendly fire. Unfortunately, there are times when the immune system makes a mistake and in the setting of this mistake the immune system will start to identify a part of the individual, a part of you that is foreign. This is called autoimmunity. The immune system attacks yourself and what we call the disease or the disorder simply is related to where the system attacks you.  For example, if the immune attack occurs in your joint, we call that rheumatoid arthritis. If the immune system attacks the pancreas of a child, we call that type I or childhood onset diabetes. If your immune system attacks the gut, we call that Crohn’s disease.  Now, when the immune system targets and attacks the brain and the spinal cord, that’s multiple sclerosis. It’s an unrelenting attack by the immune system on the brain and spinal cord. 

Now, we have to keep in mind a couple of things about the brain. I might be a neurologist and I a little biased, but the brain is pretty cool and it has the ability to adapt. It’s called neuroplasticity. It can work through problems. If there is an area of inflammation in the brain where the immune system has beat up a part of the brain, your brain will work around it. It’s kind of like driving a car down the road and I’m calling you from Columbus, Ohio. Unfortunately, we have a lot of potholes in the winter and I’ve never seen an Ohioan drive down the road and stop the car when there is a pothole and get out, call the city, and say, “Hey we got a pothole here.”  On the contrary you just drive around it, people go on the berm, on the other lane, drive over it. The brain does the same thing.  So, if the brain is trying to send a message from point A to point B and there is an area of inflammation where the immune system has attacked the brain, you’re brain will just move around that area and connect the information from point A to point B. You as a person will never know it. You won’t experience a symptom.

You experience a symptom which we call an MS attack or relapse when the area of inflammation is in a part of the brain where there is no work around.  It’s not uncommon that people present with multiple sclerosis after having lost vision in one of their eyes.  We call that optic neuritis.  The reason that it’s such a common presentation is because the optic nerve is a tiny little pathway, it’s like a thin wire. And if there is inflammation there, there’s no way to work around it.  It’s kind of like if I use the pothole analogy. It’s like driving down an alleyway. You got a building on the left and a building on the right, there’ no wiggle room. If there’s a pothole there you do have to stop the car, the patient all of the sudden can’t see, and that brings you to the attention of a clinician.

Now, that description of MS leads us to understand several different things. In my opinion, the most important is the fact that during periods of clinical quietness the disease is not at bay. To be honest with you, the term relapsing-remitting MS is maybe not the very best of terms because I think it gives a false impression that if you’re not having a relapse you’re in remission, and unfortunately that’s far from the case. I like to remind my patients that the immune system doesn’t take a nap, it doesn’t go on vacation, it doesn’t take a coffee break because it’s constantly attacking your brain and spinal cord. The medicines that we now have available today, the so-called disease-modifying therapies are intended at slowing down that process, and we’ve gotten increasingly good at it. 

I’d like to spend a few minutes and review some of the first five medicines and then I’d like to spend the rest of the time talking about sort of the newer drugs and what’s coming on the horizon.  First five medicines are injections, no pills, and they come in two flavors – interferon and glatiramer acetate. The interferons, there are three or four different kinds and I want to talk briefly about what an interferon is and what it does.  Now, the reason it’s called interferon is because it interferes with the viral replication, so when you get the flu bug your own immune system makes interferons to fight the flu.

We use interferon in MS for a completely different reason. An interferon when injected into the body has an interesting effect where they tighten the blood brain barrier. Remember a few moments ago I shared with you that these naughty autoreactive cells that are in the bloodstream, go into the brain, and cause a ruckus. Well they have to get into the brain in order to do so. They have to pass through a barrier, and some clever anatomist called that the blood brain barrier. Well, interferons tighten up the blood brain barrier.  You have to pardon the three year old analogy, the age of my son, actually he turned four today.  I read a lot of three little pigs to him, so here’s a three little pig’s analogy. Taking an interferon is like going from the straw house to the stick house, as it relates to tightening of the blood brain barrier. As a result, less of the naughty auto reactive cells get into the brain and as a result there’s less disease activity. 

Interferon comes in 3 different flavors - there’s low dose, low frequency, code name Avonex; high dose, high frequency Betaseron and Rebif; and recently joining a drug called Extavia.

Now, a separate category of medicines still first line in my thinking is glatiramer acetate (Copaxone). Glatiramer acetate works by a different mechanism. It doesn’t tighten up the blood brain barrier. What it does is it retrains the naughty auto-reactive cells in the bloodstream to be less aggressive, to be less inflammatory.  Glatiramer is nothing more than four amino acids, in a random order, in a top secret ratio that nobody knows about except for the makers of the drug. These amino acids look like myelin, they look like the plastic coating on the wires of the brain, and that’s one of the major targets of the immune system in a patient with MS. What you do with glatiramer is you inject it into your body on a daily basis, and continually, constantly, and unrelentingly remind your immune system to take a peak and look at this stuff.  Eventually your immune system quite literally becomes bored and it shifts its response to myelin from a pro-inflammatory, “Let’s go down into the bar and cause a bar brawl” to an anti-inflammatory “Let’s just stay at home, watch a TV program, maybe pop some popcorn, and relax.” As a result, when those naughty cells that are now a little less aggressive go into the brain they cause less of a ruckus.

Now and maybe in about two minutes, I’ve just summarized two decades worth of intense research. The result being these medications which we’ve been using for the last decade, decade and a half are moderately effective. They’re good medicines and they have tolerable side effect profiles. The most common side effects associated with interferon are flu-like symptoms.  Remember I shared that your body makes interferon when you have the flu and the reason you feel flu-like isn’t because of the bug, it’s because of the interferons in your own body.  Stands to reason that if you inject yourself with interferon it makes some patients feel flu-like.

Less common side effects include changes to the liver enzymes, they can elevate them, and changes in the bone marrow. Those are uncommon but require laboratories to be checked.  Glatiramer has a different set of side effects. It doesn’t cause flu-like symptoms or doesn’t affect liver enzymes, but you get a welt where you inject yourself. If you inject yourself for a long time, I’m talking five to ten years, you can get divots in your skin where you kept sticking yourself with a needle and that’s called lipoatrophy.  It’s seen commonly in folks that take insulin on a regular basis.

The last side effect associated with glatiramer is a systemic reaction, which is rather scary if you don’t know to look for it. It happens rarely. It happens in less than 10% of all people who take the medicine, and what will happens is they inject themselves and within about a minute they feel horrible - chest pressure, shortness of breath, sweating, and fear. It kind of reminds me of  Sanford and Son and when he would grab his chest and say, “I’m coming Louise.” It’s not a heart attack and it’s actually not dangerous at all.  What’s happening is an immune response and generally speaking if it happens once it doesn’t happen again. I warn my patients about it, so they know they’re not having a heart attack because they just gave themselves their shot. I tell them if they’re out shoveling snow and they have pressing chest pain, then that’s a different story. 

Now, in the mid 2000’s another drug joined the armamentarium called Natalizumab (Tysabri). This is not an injection, but an infusion. It’s taken every four weeks and it’s a potent medication.  Natalizumab has never been compared head-to-head to the first line agents. It’s been compared indirectly.  There is amassing evidence that it may in fact be a more efficacious medication, although I can’t say that definitively because we haven’t done the PepsiCo Challenge.  Nonetheless, it’s a very, very good medicine. It’s a medicine that in my own clinic, I often times use as second line therapy when my patients don’t respond to the first line. 

It has two major side effects. One of them is an infusion reaction and any time you infuse something into your body that’s foreign your body can react to it, and if that happens sometimes you can’t use it or you have to give it slower.  More concerning is the risk of an opportunistic infection called PML. PML is a virus, well there’s a virus called JC virus that can cause this PML, and the truth is about 60% of all human beings have JC virus. We actually have millions of viruses and we don’t care. We beat them up all day long because our immune systems constantly find them and attack them.  Well in certain situations when the immune system has been altered, what can happen with these opportunistic infections is the viruses go unchecked, so they can rear up their ugly heads and they can cause ruckus. PML is a serious infection. Fortunately, only 95 people on planet earth, with MS, on Tysabri have developed this infection. And that’s out of almost eighty some thousand people that have been exposed to medication. It’s never happened in the first year.

Uh, and to share an exciting piece of research with everyone on the phone, there’s a new blood test, which has been developed and is now in testing. This blood test allows us to screen for the presence of antibodies against the virus.  In other words, we can check and see if you’ve been exposed to JC virus. And here’s a pretty decent theory: if you’ve never been exposed to the virus, you can’t get PML, and this is being tested.  I am very proud that our center is one of the sites that are offering this blood test to our patients.  I think that very soon it will be validated, and it will become a commercially available test approved by the FDA. 

What it’s doing to Tysabri is interesting. It’s turning Natalizumab into, kind of, almost two different drugs. The way you treat people with and without JC virus is kind of becoming two separate groups of folks, and Natalizumab has helped many, many patients. It certainly has helped many of mine.

Up until September 22nd of last year that was the FDA approved MS armamentarium. Our stage left is a new medication called Fingolimod (Gilenya). Fingolimod is an exciting agent, it’s a pill, and it’s exciting to take a pill instead of a shot. Although, I remind my patients that I don’t pick the medicines based on how easy it is to take. I pick the medicine based on the efficacy and how well you can put up with it.  That being said, Gilenya is a pretty, a pretty exciting drug.  Its mechanism is unique and is actually the first drug in a whole new class of medications called S1P receptor-modulators.  What this drug does is kind of cool. Now follow along with me please and imagine that white blood cell that we talked about earlier is a car, and imagine that the bloodstream that it’s traveling in is a road.  Now imagine that the lymph node is a garage and what happens normally is your white blood cells goes through the blood stream and goes in the lymph node. In other words, the car drives down the road into the garage, entering the garage is free, it doesn’t cost anything, there’s no guy taking tickets, there’s no arm that goes up or down, you just drive in.  However, if you want to leave the garage you absolutely are required to show your hang tag, and if you don’t show your hang tag buddy, you are not leaving the garage.

Now, what Fingolimod does is it causes the white blood cells to swallow the hang tag. In other words, it hides the hang tag in the car. So the white blood cell drives into the garage, goes in the lymph node - no problems, but when it tries to leave it can’t. It’s literally trapped.  It always makes me think of that song Hotel California - you can go in anytime you want, but you can never leave. It traps white blood cells in the periphery in the lymph nodes of the blood stream. Well if they’re in the lymph node, they can’t get back in the blood, if they can’t get in the blood, they can’t cross the barrier into the brain, and they can’t cause a ruckus. That’s how Fingolimod works. 

Fingolimod was tested in two big trials. One of them called the TRANSFORMS trial was a one year comparison against a known agent, low dose, low frequency interferon, and Fingolimod faired better. It decreased relapses better than interferon did.  There wasn’t a difference in disability. You know we can talk if someone has a question about why that is.  There was a second study done that we participated at Ohio State University called the FREEDOMS trial. The FREEDOMS trial was a comparison against placebo, against a dummy pill. They showed very nicely that the drug outperforms placebo quite handsomely, decreases relapses quite substantially, as well as decreasing disability. So, we now have this new medicine that’s available as part of the armamentarium. Now a bigger dog has a bigger bite. And Fingolimod or Gilenya has side effects that need to be grappled with.

It turns out that those hang tags, those S1P-receptors aren’t only located on the white blood cell, they are actually all over the place. You have them on the heart, on the smooth muscle of the bronchioles, the tubes going down to your lungs, there’s receptors on the skin, and the back of the eye.  As you can imagine there’s a lot of potential side effects. Now, what that translates into as it relates to my patients who have recently started the medication is a lot of testing to get ready to take the medicine.  In my clinic prior to starting the medicine, I require my patient to get an EKG and I require them to get pulmonary functions tests (PFT), so that I know their baseline heart function and lung function.  I require them to see a dermatologist and an ophthalmologist. That’s not required by the FDA, but I feel that it’s important in my clinic to have that level of surveillance.  We also have to check and make sure that they’ve already been exposed to the chicken pox family of viruses, and if they haven’t we have to immunize them.

After jumping through all those hoops then comes the big day. I was fortunate to have a patient who had his big day today. They come in the clinic first thing in the morning. I literally watched him swallow the pill, and then we have to follow them for the next six hours because only the very first day when you take Fingolimod it can drop your heart rate on average about eight beats per minute, which is not significant. It can continue for about four to six hours. In 5% of the patients in clinical trials their heart rate actually got below 50, and about 5% of people were aware of it and had problems. So, we need to have close and careful monitoring.  Fingolimod is being used in the MS world increasingly and we’re still struggling and trying to figure out where exactly it fits. 

Currently, at least in my center we’re using it not often as a first line agent, but more often as a second line agent when you haven’t done well on the injections that I’ve described before you.  But things don’t stop there, folks. We actually have many, many other drugs that are coming down the pipeline very rapidly.  There’s two pills. One is called Teriflunomide and this is a medication that has completed a phase three test and it worked.  The numbers weren’t as fancy as what we saw with Fingolimod, but it was a successful medication - decreasing relapses and decreasing disability. It’s also a pill you take once a day.  Now, this is a pill derived from a chemotherapeutic type agent and it’s absolutely a no, no to even say the word pregnancy around it. You wouldn’t want to get pregnant on the medication. However, aside from that serious issue it didn’t have side effects that were outside of what we were used to seeing with the placebo. This medication has yet to go to the FDA, but I think it will very soon. 

There’s another medication called Laquinimod. I don’t know who makes up these names, but I’d love to talk to them cause they’re pretty creative. Laquinimod is also a pill you take once a day and it’s completed its stage three testing.  There was a recent press release that shared that it was a positive trial. The drug works in slowing down MS, but we haven’t been graced with the data to know exactly how it works and I think that’s going to be released very soon, maybe in the next couple of months.

There’s many other drugs that are coming down the pipeline. There’s another pill actually called BG-12, which is probably a pill you take two to three times a day. It’s still being tested, but uh, the preliminary data looks amazing - very, very encouraging. If you leave pills aside and you think about infusions, there’s many other medications that are being tested. 

Now, think back a second ago, I talked to you about a medicine called Natalizumab (Tysabri). Tysabri is in a class of medicines called monoclonal antibody. Monoclonal antibodies, it’s easiest to think about them as smart bombs.  Think for a second of MS as a factory - machine A, goes to machine B, goes to machine C, goes to oh you have MS. What these smart bombs do is that they target one of the machines and they break it. So, if they break let’s see machine B, you go machine A 'wa wa', and then everything stops. That’s how these medications work. 

Again going back to Natalizumab, the way that Tysabri works is it tightens up the blood brain barrier in a way that we haven’t seen in the past. It’s kind of like going from the straw house with the three little pigs to the brick house. It prevents the white blood cells from leaving the bloodstream, so the naughty ones can’t get into the brain and cause a ruckus.  It turns out there are many other monoclonal antibody (smart bombs) that are being studied.

There’s a medication called Rituximab. This is a medication that recently completed an exciting trial looking at the less common form of MS called primary progressive MS, and in a subgroup of those patients we were actually able to show that it slowed the disease down. Rituximab is unique in that it actually works on B-cells.  Your immune system is made up of both T-cells and B-cells. Most everything I’ve talked about so far affects the T-cells. Rituximab is one of the first medications that targets B-cells and we think what it does is it interferes with the chit-chat between the B-and T-cell. If they’re not allowed to talk, the T-cell doesn’t know what to do, and it doesn’t attack. Rituximab has been studied and both the more common type of MS, relapsing-remitting MS, and the less common. There’s good data preliminarily that it seems to work. 

Now there’s two derivatives of Rituximab that are under investigation. One of them is called Ocrelizumab and that’s entering into phase three testing now, so it’s going to be several years before we see the results. There’s another drug that’s hard for me to say called Ofatumumab. I’m being serious, I didn’t make up that word. It’s also a B-cell agent, so B-cell agents and B-cell monoclonal antibodies are picking up steam.  I think we’re going to see them joining the MS drug list very, very soon.

There’s another monoclonal antibody called Alemtuzumab, code name Campath. It’s actually been around for a long time to treat certain types of cancer and it’s maybe the biggest smart bomb we’ve ever seen to date.  It’s a medication that targets any cell that has a particular hang tag called CD52. It turns out that almost all the white blood cells have that, so when you give someone Alemtuzumab, the result is profound.  It’s kind of an interesting medicine. It’s an infusion you take for five days in a row and then you don’t do anything for the rest of the entire year.  The second year you take it for three days in a row and then you don’t do anything. This medicine when it was tested it was pitted against one of the interferons, and it outperformed the interferons in a way that we’ve never seen before.  Suffice to say that there’s a lot of very, very exciting agents coming down the pipeline and choices are wonderful.

It’s easy for me to talk about large groups of people. You know I can quote you statistics about a group of people that were in this trial, or that trial, but let’s be honest when I mean clinic I’m not talking to a group of people. I’m talking to one person who has a name and a family. My job as I see it is to help that person live a healthy and exciting life as possible, and not to let MS get in the way. I’d like to switch topics and talk about how I try to accomplish that because it doesn’t really depend on which drug you’re on.  My contention is that it doesn’t take a rocket scientist or brain scientist to identify someone with MS, and to say, 'Hey, this person with MS needs to go on a therapy.'  I think that message has largely caught on, and that people are started on therapies early and try to maintain on therapies.  I think it takes a really keen observer and a really good listener to identify when a patient is not doing well, when the drug is not successful, and knowing that it’s time to make a switch.

Now speaking broad strokes, here’s how I try to go about that during my clinic.  I tell my patients there are three things that I use to try to help guide us to determine if their medicine, their disease-modifying medicine is doing the right job.  The first one and one of the most important one is what the patient tells me. The patient is with themselves all day long every day. I only see them maybe 4 times a year, and so I have to be a good listener when the patient says, “Look doc, I can’t do x, y, or z and I used to be able to” or when the patient says, “Yeah, 3 weeks ago I have this problem. I couldn’t move my leg and it stayed that way a while.” I’m thinking oh my goodness they had an attack and why didn’t they call me earlier.  The second way that I learn about how they’re doing and how they’re drug is helping them is by examining them.  I’m a little old fashion I actually like to examine my patients thoroughly and I look for changes. If you develop a limp, and you’ve had a limp for couple of months you might forget you have it, but I haven’t seen you in a couple of months. I wrote it down what I saw last time, and so when I see that left leg dragging I say, ‘wait a second what’s going on there buddy?’  The third way, in order of importance, number three, is the MRI.  I don’t treat MRI’s. I treat people, but the MRI gives me insight into how things are going. Let me explain what I mean. 

One of the first comments I made to you this evening was that during times of so-called remission you’re still being attacked, your brain is still being attacked by the immune system, and you might not be aware of it. The MRI can pick up those attacks. When you get an MRI and there are new spots on the scan, new white spots, new lesions, I mean there’s a lot of terms we use. What that tells me is that the immune system has successfully broken through the barrier and attacked the brain, and the reason you didn’t know about it is because it wasn’t in an area where it caused any symptoms.  I’d like to get MRIs on my patients that are doing well about every year, maybe upwards every year and half or so. What I am looking for isn’t the fact that they had one new spot; it’s the change over time.  I’ll give you an example:  If patient A had a hundred spots on their brain and a year later they have a hundred and ten spots, I’m actually a lot happier about how things are going compared to patient B who had ten spots in year one and twenty spots in year two. Patient B has actually doubled the number of spots they’ve developed, their delta, their change over time is much more pronounced. 

As we follow our patients in my center, we use these three rubrics to kind of help decide how the drug is working, and I tell my patients when you go out with a drug you’re really going out with a drug - you’re dating. You see how things go.  You know he drives a nice car, it’s clean, he looks dressed up, he’s polite, he opens the door for you, you go out dancing, and you have a good time. You say, “Yeah I’ll go out with you again.” If things go well you start to go steady.  If my patient’s disease is kept at bay and they tolerate their medication, I want them to go steady as long as they can, if not forever, or until I find a better drug or I can figure out a way to slow the disease down better than we’re doing. When the disease is picking up speed well that drug is no longer behaving himself, and I tell my patient it’s time to break up. You got to give him his keys back, you got to take his number out of your cell phone, you unfriend him on Facebook, and you tell him, “Look it’s not you. It’s me. I need some space,” and then you never call him again.  We drop that drug and we go to a different one in hopes it’ll get a better control over the disease.

Now, if I can ask the moderator how we’re doing on time. Kasey are you back there somewhere?

Kasey Minnis: We are at about 7:30 right now, so if you’re ready to begin questions?

Dr. Boster: Let’s do that. Um, I will ask folks that it’s hard for me to answer specific questions about your particular situation because I’m talking to you on the phone. I can’t see or examine you.  If you can please ask your questions in a more general way that would apply to the whole audience, that‘ll be really helpful. And with that caveat please let’s have at it.

Kasey Minnis: Okay folks, to ask a question you need to hit the star key and the number one on your phone. As questions come in, I will call on you by your city and state and you will hear on your phone that you have been taken off mute. Alright, we’ll start with a question from Garden City, New York. Garden City your question.

Caller (Garden City): Ok, what role does stem cell play to repair the damage that’s been done? And when are they going to get going with it?

Dr. Boster: Nice to talk to you. I hope your weather is better than mine here in Ohio. Your question has to do with stem cells and there’s actually a deeper question underneath, which is neuroprotection, neurorepair. Almost all the drugs that I’ve talked about to date do a good job of decreasing inflammation, but we know that there’s an underlying process which is neurodegenerative. It’s a degenerate process of the brain, and that’s really what we want to get a hold of.  Now, you said when are stem cells really going to pick up steam?  We’ve actually been studying some cells for over, over 8 years now. It’s being done in the setting of  research studies.

There are large registries that have been collected in Canada, there are large registries that have been collected in Europe, and there are small projects going on at various academic centers in the United States. Ohio State is one of them.  We are participating in an exciting trial called the HALT Trial, which is a stem cell transplant trial.  Now, what I’ll share with you is the following: Number 1 - I genuinely do not believe that stem cell is a cure to multiple sclerosis.  You know when you give medicines, particularly when you give chemotherapy type medicines to an MS patient. What you are trying to do is, you’re trying to do a soft reboot to the immune system, kind of turn it off, and let it restart. You hope that when the cells come back they’re less naughty.  When you do a stem cell transplant it’s like doing a hard reboot, it’s like swapping up the mother board. You literally remove the patient’s immune system and you give them a different one in hopes that that immune system behaves itself.  Now, at first blush that sounds like it might be a cure, but what we’ve learned from the clinical trials thus far is that patients can still have ongoing disease activity, their brain still atrophy, and the disease does continue in some cases.  I’m excited about stem cells, but it’s not prime time. It’s nothing that I would ever recommend one of my patients do outside of a controlled clinical trial. Thank you very much for asking that question Garden City.

Caller (Garden City): Thank you.

Kasey Minnis: All right our next question is from Joilet, Illinois.  Joilet you’re on the line.

Dr. Boster: Howdy!

Caller (Illinois): Hi there. Thank you for being so kind with your time and talking to everybody.

Dr. Boster: You honor me. Thank you, sir.

Caller (Illinois): When is it appropriate to treat CIS and RIS? In people, you know, could you explain that? That’s all I had to say. Thank you again doctor for your time

Dr. Boster: Great question! Great, great question!  So, the gentleman brought up an exciting area in MS and one I’m particularly interested in.  So, let’s define those terms for everyone on the phone.  CIS is doctor talk for clinically isolated syndrome. Now what the heck is that?  Clinically isolated syndrome is what we call the first attack of multiple sclerosis.  So the way that we used to define the disease is you had to have at least two attacks, you had to have at least two bad things happen to you, they had to be in different places of the brain, and they had to occur at different times. So, it stands to reason that when you had the first attack you don’t have the diagnosis yet because you haven’t had the second. Right? And we call that first attack clinically isolated syndrome. 

Now because of work largely done out of the Queen Square Group, and a consortium of amazing doctors, and the Magnus Group in Europe, we’ve learned a tremendous amount about CIS (clinically isolated syndrome). It turns out that if you have the first attack of what smells like MS, what looks like it’s going to be MS, and you have a normal brain MRI, then your risk to develop MS over the next 20 years is about one in five, twenty percent.  Now, keep in mind that in Illinois the risk of getting MS is about one in 700 - that’s a lot higher.  However, if you have a clinically isolated syndrome, the first attack is probably going to be MS. You get a brain MRI and there’s spots on the brain that look like MS spots. Your risk to develop MS over the next 20 years is actually 85%. That’s a really high number, and to answer your question directly, when do you treat CIS? 

Sir, I don’t actually think CIS exists. I think CIS is simply an observation at the beginning of MS. When I see a patient with a first attack and with spots on their brain, that’s multiple sclerosis and I initiate treatment.  Moreover, the same imaging group that I talked about, the Magnus Group has recently presented us with new diagnostic criteria for MS.  And many things that we used to call clinically isolated syndrome actually now meet criteria to be diagnosed as multiple sclerosis.

So to summarize, if you had your first attack and your brain MRI tells us stuff is going on, I think the better part of valor is to begin treatment immediately.  Now, the second part of the question was, when do you treat RIS?  RIS is even more (ha ha) complicated. It stands for radiographic isolated syndrome. Now, it so happens people get MRIs for all kinds of different reasons - maybe you had a headache, maybe you banged your head, or for whatever reason the doc put your head in the scanner and gets a picture not because he or she suspects multiple sclerosis.  Sometimes when that happens you’re shocked at what you see and you say, 'Holy moly, this brain looks like the person has MS.' Except when you talk to them, when you examine them they’ve never had an attack, and they have nothing on their exam to support that.  This is a very contentious topic and I think that a solid MSologist and a patient need to come to a solid understanding. At bare minimum, I think those kind of patients need to be surveyed with serial scans and serial exams.  Thank you for that question.

Kasey Minnis:  OK. Our next question is going to be from Aiken, South Carolina.

Dr. Boster: Hello!

Caller (Aiken, SC):    Hello. Thank you for being so funny.

Dr. Boster: Hahaha, it’s my pleasure ma’am.

Caller (Aiken, SC): I love your little piggy story. Um, I have an odd question, and I hope that it’s not too weird…

Dr. Boster: Oh, I’ll provide an odd answer. Feel free.

Caller (Aiken, SC): With a great saying with it I’m sure. Um, I take Copaxone and when I go to my support groups everybody 'poo poo’s' me. It seems that you either are on the Copaxone team or you’re on the interferon team.  Can you tell me in one of your clever little ways, what’s the difference? I mean it’s working for me and I haven’t had an eye issue since I started it, but they always make me feel as I’m taking the wrong medicine.

Dr. Boster: I understand.

Caller (Aiken, SC): OK.

Dr. Boster:  But I think the issue lies that you’re going to the wrong support group.

Caller (Aiken, SC): Hahahaha.

Dr. Boster:  Now, the drug that works for you is the drug that works for you.  I think it’s important to keep in mind a couple of things.  Number one, you’re not a statistic. You’re not a group of a thousand patients in clinical trial. You’re an individual, right? And you’re on a medicine to slow your disease down, you guys have been dating for a while now, and things are nice. I mean he still brings you flowers, he’s polite, and he remembers your birthday. This is a good guy and he’s doing well by you, and for you this drug is working?

Caller (Aiken, SC):  Yes.

Dr. BosterNow, probably for political reasons as much as anything else, you’ll find camps of doctors (guys and gals) who really dig one drug and really dig another. I think that’s just part of human nature if I’m honest. In the late 90’s, excuse me, mid 2000’s there was an effort made that tried to clarify whether one drug was better than another, the so-called Pepsico Challenge. In fact, there were three trials. These were really large experiences; hundreds of millions of dollars were spent to try to do a Pepsico Challenge of glatiramer acetate (Copaxone) with one of the interferons, the high dose interferons. The attempts were made to prove that the interferons were superior to glatiramer.  Now, the results of these trials largely demonstrate that there was no difference and that the investigators were not able to prove that the interferons worked better. OK? So I guess the first thing you tell your support group is, 'Leave me alone. I’m doing well in my disease.' That’s a reason to have a beer and just say, 'Thank you.'  Number two is you tell them the research does not support what you’re saying. Number three is you remind everyone that everybody is an individual and your immune system is genuinely unique to you. There isn’t a soul in the world that has an immune system like yours. The nervous system, the thing that is being attacked by your immune system is hands down one of the most complicated organ systems in the body. When you throw the two together, mash them up, and see what happens, it’s different for every individual. If you and your clinician have stumbled upon a medicine that works well for you, fantastic. You wouldn’t want to change that.

Caller (Aiken, SC):  Thank you.

Dr. BosterReady for the next question?

Kasey Minnis:  Thank you to our friend from Aiken. Now our next question is going to be from Jacksonville, Florida.

Dr. BosterHello, Jacksonville!

Caller (Jacksonville):  Hi! Am I on the air?

Woman Speaker:  You sure are!

Dr. Boster:  Yes, ma’am.

Caller (Jacksonville):  Okay, my question is about Methotrexate.

Dr. Boster: Aha.

Caller (Jacksonville): Yeah, my doctor, neurologist recently put me on Methotrexate and I have not been on any drugs before that. I’m just wondering what your opinion of Methotrexate is in using in patients who present with, ah joint pain, or kind of … to me it feels like arthritis in the hips, you know?

Dr. Boster:  Gotcha, gotcha.

Caller (Jacksonville): How Methotrexate would, do you think it would help because I’m not getting much, I don’t feel like I’m getting much benefits from it.  I’m at seven and a half milligrams…

Dr. Boster:  Sure.

Dr. Boster:  Methotrexate for those of you that are not familiar on the phone is a pill. It’s a pill that’s been around for a long time, it’s a form of chemotherapy, a form of immunosuppression. It works by suppressing the immune response and by killing off some of the white blood cells, so they’re just a little less aggressive. Methotrexate is used in several different kinds of autoimmune conditions like rheumatoid arthritis, as you just mentioned.  Now, in multiple sclerosis it was one of the oral medicines that were used prior to the discovery and advent of the injections. And it’s, it’s not something I use in my personal practice, but you know there’s a reason they call it the art of medicine. There are many MSologists out there that will add something like an oral immunosuppressant, in addition to one of the injectable medicines or they might chose to use it differently.

I can’t speak to your specific situation, and when you tell me about joint pains it makes me say, ‘Whoa you got to talk to your doc.’  MS can do many, many things, but it doesn’t cause joint pain.  Now, it can cause joint pain if you have a weak leg and you’re limping, but it doesn’t primarily do that. So, I think these are one of those situations where it’s very important you sit down with your clinician and you get him or her to explain to you their rationale.  It’s very important to me that a patient understand why they’re on a medication and they agree with the medication.  I have this belief that you are the boss of you. I’m not the boss of you and just because I’ve read some books that you didn’t read doesn’t make me the boss of you.  I view my role is to help educate you to make a really good decision, and sometimes your decision isn’t what I would pick, but that’s okay cause it’s your disease and not mine. This is one of those cases where I would encourage you to sit down with your clinician and say, “Come on man and break this down for me. Make sure that I understand why we’re doing what we’re doing.”  Thank you.

 Kasey Minnis:  Our next question is from Lincoln, Nebraska.

Caller (Nebraska):  Hi! Um, I have secondary-progressive…

Dr. Boster: Aha

Caller (Nebraska): Um, is the story in your mind very different from people with secondary progressive?

Dr. Boster:  So, thanks for the call and for the question. Um, secondary-progressive MS, let me explain what that means.  The relapsing form of MS, relapsing or remitting MS is the way 85% of all people with this disease present. They have an attack and then they go through a period of time where they’re not having an attack, then they have another attack, and so and so forth. Now, most patients particularly left untreated, but most patients even treated will eventually change the way their disease behaves. What happens is they stop having attacks or at least they don’t have them very often and yet they develop disability. They develop problems separate from attacks.  Um, a good example might be a gal that used to golf 3 times a week. She’s pretty good, she’s on a golf club, and over the years she had to stop golfing, so often she went from 3 times a week to once a week. She had to quit her club because she couldn’t keep up. It was hard for her to walk the distance, she limped. Then a year ago she actually had to stop golfing completely, and then in the past six months she is now borrowing her husband’s cane. So in that example this is someone who not because of an attack, but because of slow progression has actually started to accumulate disability.  That’s how I think it’s helpful to think about secondary-progressive MS. 

Now, when we look at the medicines that I’ve discussed with you in pure secondary-progressive MS, I say with humility in my voice that they have not shown to be helpful.  It’s not for lack of trying and it’s important to keep in mind that that’s in a large group of people.  Now, you can only determine that someone has secondary-progressive MS retrospectively. Think about this for a second.  I just told you a story about something that happened to a golfer over the past five years, but when you’re standing at time point, now zero, looking forward you don’t know what’s going to happen. You might have an attack the next day. I feel strongly. I don’t practice medicine in a socialized or capitated system and if I have a patient with relapsing disease I will treat them. It’s only after the patient and I am absolutely convinced that the disease has entered a progressive phase without any relapse, any suggestion, hint, or inkling of a relapse that we might talk about not using that therapy. 

To answer that question more directly, a tremendous effort has been made in trying to find a drug to slow down progressive disease, both primary and secondary-progressive. That’s kind of the holy grail of MS. To be honest with you we’re still working on it.  There are many, many things that you can do to help someone with secondary-progressive or primary-progressive MS.  Everything I’ve said tonight is geared towards disease-modifying therapies, but there are two other ways that we treat MS. One of them is a relapse. How do you treat a relapse?  We’ll talk about that if someone asks the question, but the other way is symptomatic management.  Now, treating a symptom doesn’t slow the disease down, but it doesn’t speed the disease up fortunately.  Treating a symptom improves quality of life and I make a joke with my patients that I have a pill for every ill. It doesn’t mean I give them a pill for every ill. It just means I know the name of one, and we decide on case-by-case basis what ails the patient and what they feel is bad enough that they want to take a medicine for.

Now, uh, there’s another pill that was recently released in the market last year called Dalfampridine. It used to be called 4-aminopyridine with the trade name, Ampyra.  This is a medicine that I’ve actually been using for years off label in compounded pharmacies (old school pharmacies) that still make medications, but it’s now FDA approved and available through your insurance company.  This is a symptomatic therapy and it does not slow down the disease, but it treats two remarkably important symptoms that a lot of folks with secondary-progressive MS suffer from. Symptom number one is motor fatigability. 'Doc, I used to be able to walk the distance of the mall. Now I get about the equivalent of a city block and my legs become weak. I can’t go on. I have to sit down and rest. If I rest for a while I can do another block.'  That’s motor fatigability.  A second symptom that it helps is heat sensitivity.  Heat sensitivity doesn’t mean that I dislike Columbus, Ohio in August, which I do strongly by the way. What it means is when my body gets overheated, when my core temperature raises because I have a urinary tract infection or it’s god awful hot in Ohio in August or because I have a fever because of some other cause or I’m sitting in a sauna, my old symptoms come back to visit me.  All the stuff that has happened in the past, the optic neuritis that left me blind in my right eye, which got better, or it comes back and now I can’t see. That’s reversible when the core temperature drops. 

In about one third of people with these kind of symptoms, the medicine Dalfampridine makes that better. So my patients when they respond they can walk farther. When they get overheated they don’t go blind and that can really improve a guys or a gal’s quality of life.  Stay tuned though there are a lot of things in the pipeline. Many are geared toward progressive disease and we’re trying real hard.  Thank you for the question.

Kasey Minnis:  OK, we are just under ten minutes left. Our next caller is from Newton, Connecticut.

Dr. Boster:  Hello!

Caller (Connecticut):  Hello doctor! Thank you so much for being here.

Dr. Boster: My pleasure.

Caller (Connecticut): I have a question about symptoms that I’m feeling, yet they may not show up as white spots on an MRI. What does that mean?

Dr. Boster:  That was a wonderful question and it brings up a very important topic. Thank you for asking it.  Remember little bit ago when I said there are three things I need to do to sort out how a patient is doing? I shared with you the first one. The number one symptom or the thing that I need to pay attention to is what the patient tells me.  I have this belief that you actually know your body better than anyone else because you’re in it all day long, and it’s true that many times a symptom may not correlate to a spot on the MRI. There’s actually a fancy term for that and we use it in this field called the clinical radiographic paradox, which is exactly what you just described, “I’m having a problem but it doesn’t show up on my MRI, so what’s the deal?” Well the deal is as follows:  MRIs are not perfect tools. The MRI machine, the standard MRI, when your doctor hands you a prescription, you go to the scanner, you go in the tube, it’s real loud, you come back out.  The MRI machine takes a picture of fat and water, so you get a great picture which is awesome for brain imaging because our brains are largely made up of different types of fat and water, and so we get really nice pictures. 

Now, if there’s an area of inflammation it’ll cause an increase in water. I mean think about when you bang your elbow and it swells up, that’s inflammation, that’s bursitis. There’s lots of water in there. The same thing happens in the brain, when you take a picture. In other words when you get an MRI it shows up as a bright spot.  The problem is that there’s lots and lots of other damage to the brain, which the MRI machine can’t see.  I’d like to use this analogy to make that a little clearer or at least I hope it makes it clearer.  In the room that you’re sitting in there is ultraviolet light in the room and there’s also infrared light in the room, but you can’t see it. Your eyeballs are only set to see certain wavelengths of light.  Now, if for some strange reason you had a pet bat, had a pet bumble bee, or you had a pet snake; these animals have different eyeballs and their eyeballs are set to see different wavelengths of light.  The MRI machine is set to see certain types of problems, water-based problems, but it’s not set to see other problems. 

Fortunately, we’re diligently working on other MRI metrics, other MRI tools that allow us to see more.  There’s a host of what we call non-conventional imaging. Non-conventional meaning it’s not the standard stuff you get when you write a prescription and just go to the scanner.  These are largely done in research and they include looking at atrophy and shrinkage of the brain. They include looking at the gray matter of the brain which was ignored until maybe about a decade or so ago, they look at the integrity of the myelin, the plastic coating on the nerves, the wires of the brain, and they look at the metabolic activity or the functional activity of the brain in unique ways.  Now the good news is these tools are being applied readily in clinical investigations, and once we get them worked out, I anticipate that some of them will be used in the clinic also.

The second thing that we have to talk about in this clinical radiographic paradox, this issue of “I have a symptom and it doesn’t show up on my scan” is our ability to do an exam and document disability, but it’s not perfect. Right?  Our ability to do an exam and tell you what’s going on is really, really good, but it’s not perfect.  In the scales that we use, the EDSS is this scale that we’ve all become married to, that we use when we assess a patient and we look at their level of disability. It’s an imperfect tool.  We try the best we can. Please keep in mind, that we’re practicing the art of medicine and that we don’t have everything worked out just yet, but we’ve made leaps and bounds over the past decade or two in our understanding. 

For example, at Ohio State University I’m very excited that we have a 7 Tesla MRI. This is one of the most powerful MRIs on planet earth, and when we scan patients we can see things that you can’t see with a normal scanner.  It’s kind of like the difference between the old black and white TV’s with the bunny rabbit ears. It’s kind of a grainy picture, and if you’re watching the Super Bowl you‘re not sure which guys are running the ball vs. the new plasma screen TV’s, the high definition TV’s where you can see the sweat running down his face.  We’re working with new, exciting, and more powerful MRIs that let us see that kind of resolution.  Tune in to lots of exciting stuff coming down the pipeline.  The thing that I would share with you as it relates to you specifically is making sure that your doctor is listening and say, “Look, I know it’s not showing up on the MRI, but you got to take me seriously. I got stuff going on.”  Thank you for that question. Shall we take one more?

Kasey Minnis: Our next caller is from Lake Wiley, South Carolina.

Dr. Boster: I’m jealous of where you live.

Caller (South Carolina):  Can you hear me?

Dr. Boster:  Yes ma’am.

Caller (South Carolina):  I couldn’t tell where I was being held from. Ah, I’m right outside of Charlotte, North Carolina. Um, and it’s called Clover, South Carolina.

Dr. Boster:  Nice to meet you.

Caller (South Carolina):  I have been on Tysabri infusions for 2 years and 3 months…

Dr. Boster:  Aha

Caller (South Carolina): I consider measurable benefits and no ill-effects.  I am now participating in the Stratified to JC Virus Antibody Clinical Study.

Dr. Boster:  Aha.

Caller (South Carolina):  Um, I have two questions.

Dr. Boster:  Okay.

Caller (South Carolina): How do you interpret and apply the results of the JC virus antibody test on a practical basis?

Dr. Boster:  Okay and question number two?

Caller (South Carolina):  Question number two (laughs) might be politically incorrect.  Um, the cost of the Tysabri has been consistent for 2 years and 2 months and just this last month it jumped up to two thousand dollars even.

Dr. Boster:  Wow!

Caller (South Carolina): Wondering what…?

Dr. BosterWhat happened?

Dr. BosterLet me tackle the first one because I’m able to answer that a little more clearly.

Dr. Boster:  The question that you asked is what do we do with STRATIFY. I remind the audience that one of the concerns with Natalizumab (code name Tysabri), is that it’s such a tight barrier between the bloodstream and the brain that the white blood cells can’t get into the brain, which helps slow down MS considerably. However, you need those white blood cells sometimes and there’s been cases where the soldiers aren’t present in the brain. They’re not surveying the brain and an infection like the JC virus can rear its ugly head and go unchecked. It can cause serious damage and in this case PML (progressive multifocal leukoencephalopathy) - bad news. Now, the JC virus antibody test is a fascinating test and it’s really kind of cool. 

What it does is it looks for antibodies that your body has made against JC virus.  Here’s the theory:  If you have come in contact with the virus, then your body makes a response to it.  We talked about that during the first few minutes of my discussion and that response sticks around in your body forever. If I check your blood and I see that you have antibodies against JC virus, well guess what?  You’ve been exposed to JC virus the way you know roughly 60% of people over 30 have.  Now, the question becomes what do I do with that information? I can share with you at least how I grapple with this concept and the conversations that I’ve had with my patients in our clinic at Ohio State.

Before the JC virus antibody test came about I made an assumption that everyone was JC virus positive.  I did that on purpose because I want to have a high clinical vigilance. I don’t want anything bad to happen to my patients and I want to survey them carefully.  In my clinic that means that they are seen every three months and that they have an MRI every year after the first six months. That’s how we play ball.  Now, some patients after going thru the STRATIFY test they don’t have JC virus antibody.  Theoretically, they can’t get PML.  I use the word theoretically because it’s critical that we keep in mind that this is still a research test.

I think the science is sound and I think the theories are solid, but it has yet been definitively proven. Please keep in mind that this is still a work in progress, and with that caveat if we accept it at face value, the assumptions of the study:  if you are JC virus negative, you don’t have JC virus, you probably can’t get PML. In those patients we kind of sigh a breath of relief and we say, 'Oh well, that’s good.'  Even though I continue to survey them, I do so with a little less worry. We don’t change our protocol because again this is still research. If this is proven, maybe we won’t have to survey them as often.  If you are JC virus positive, what that tells me is that you are in fact who I think you were.  You’re a person.  You have MS.  It’s bad. You need a good drug.  You’re on Tysabri and you’re doing well, and you are at risk in the second and in the third year of developing PML. At a risk, which is right now roughly more than one in one thousand.

The way that we do things is as follows:  If you’re on Natalizumab and you’re JC virus positive then before I infuse you with the next dose, you’re required to come into the clinic and sit down with either myself or one of my wonderful nurse practitioners. We have a conversation just like you and I are having right now.  Again, I’m not the boss of you and I’m comfortable giving my patients Natalizumab as long as they understand the risk and they’re willing to do the surveillance that I feel necessary.   If they’re comfortable then we just keep on keeping on, but if they’re not comfortable then we switch to something else.  It’s interesting to me, in my experience that about half of the patients on Natalizumab who turn out to be JC virus positive want to stay on and about half want to come off. I think that speaks to human nature.  Different people have different risks profiles. Some people have no problem going to Vegas and throwing thousands of dollars on the table and other people wouldn’t even buy a lottery ticket because they don’t want to lose the dollar.  It’s not my position or my right to tell you what your risk profile is.  I just want to help you make sure that you can make an informed decision.

Thank you for that question. The second question is much harder for me to answer because it has to do with a bunch of stuff that I was never taught. I guess when prices change, I immediately ask the patient to contact their insurance company to figure out what happened and remind the clinician that they can reach out to the company that makes the drug.  There are patient assistant programs associated with every single drug that I’ve spoken about tonight with no exceptions.  The company’s that make these drugs, I believe in my heart are not just out to make a buck, but they also have an interest in helping people. I think the proof in the pudding is that all these companies support patient assistance programs.  In the case of Natalizumab, sometimes they will chip in or in some cases provide free drugs if you demonstrate that you genuinely can’t afford the therapy.  I would certainly go marching back to your clinician and say, 'Let’s get Biogen on the phone in the case of Natalizumab and let’s ring them up and see what’s going on.' I would also talk to the insurance company and get to the bottom of it. 

Dr. Boster:  Thank you for that question.        

Kasey Minnis: The foundation can help you get in touch with the patient assistant program for which ever medication your doctor has prescribed. If you need assistance in finding that patient assistance program you can call one of our case workers at 888-673-6287 and they’ll help you get connected with the right people.

Dr. Boster:  Will you say that number one more time?

Kasey Minnis:  It was 888-673-6287. That’s 888-MS-Focus

Dr. Boster:  What a wonderful, wonderful service. Thank you for doing that.

Dr. Boster:  First of all gang, let me say thank you for giving me the opportunity to talk with everyone tonight. Your organization is pretty special and I think we’re all really lucky you guys are around.

Kasey Minnis:  Thank you.

Dr. Boster:  Let me share a couple of thoughts and these are things I like to share with the rest of my patients when I meet them for the first time.  Number one is in the modern era with therapies, MS is not a death sentence. You don’t die from this disease, you die with it. Number two is it doesn’t effect your ability to have beautiful, healthy children, and the risk to pass on MS to your kids is very low. It’s not like cystic fibrosis or sickle cell anemia where if you have it then one in four of your kids are going to have it.

In my opinion, there aren’t any hard fast rules about stuff you can and can’t do. I have patients that climb mountains, literally.  I have patients that are doctors, lawyers, race car drivers, cops, bookkeepers, teachers, and all walks of life.  I firmly believe that there’s no restriction in what they should do.  If MS gets in the way then we’ll work on it.  I’d like you to conceptualize the disease as an unwanted passenger in your car.  Follow me if you will. You got someone in your car and you don’t want them there and you can’t get them out. It’s not an option, but you have to make a very important decision. Who drives the car?  If you take a passive role, I promise you that MS will be happy to drive and where it drives you, you won’t like.  But you can choose to drive, you can choose to take control, and be active in your disease process. What I would recommend is you stop and get some duct tape, duct the hands of MS (this unwanted passenger) behind his back, duct tape his mouth closed, put him in the trunk, lock the trunk, and YOU drive.  That means taking an active role in your own disease process.  Let’s say, 'Okay that’s great Aaron! How in the hell do you do that?'

Number one is it’s important to become educated. I commend all of you because you’re all doing that cause you’re willing to put up with my corny jokes the last hour. Number two is you don’t get a buy from life just because you have MS. Sometimes nature is just a little too generous and guess what you still got to get up, put pants on, and go to work to the best of your ability.  My patients that do things outside of their home whether that be working, volunteering, going to classes - they do better than my patients that sit at home. I think there’s a reason and I don’t think it’s a neurological or immunological reason. I think it’s a human reason because if you are flipping burgers for eight hours, during a good portion of that time you are not thinking about your disease process.  If you’re out of the home volunteering at a soup kitchen or reading to children in a library, you’re not thinking about the fact you have something you don’t want. I think that’s very, very powerful.

The next thing I really want you to think about is the benefit of exercise. If you’re carrying 30 extra pounds on your belly and you develop a weak leg because this disease results in a weak leg in you. You got 30 extra pounds on that weak leg and that may actually result in you not walking.  If you lose 30 pounds all of the sudden the burden on the weak leg is lifted literally and you might be able to do things you weren’t able to do before.  Exercise helps MS patients with thinking and memory. It really helps patients with cognition. It helps patient’s fatigue, spacticity, and depression. These are big issues for many of my patients and a lot of people say, 'OK, well which is the exercise for me?' My response is the exercise for you is whatever the heck you can get yourself to do. I’m a realist and if you despise running then maybe that’s not what you should be doing. You really like doing yoga, do a lot of yoga.  If I had to pick an exercise, I would get my patients in the pool.  Water is magical for MS patients.  When you’re in the pool you weigh less.  When you’re in the pool and you fall to the left, the water pushes you to the right.  When you break a sweat in the pool the water literally pulls the heat off your body by convection, and spasticity in the water is reduced.  People can do things like water aerobics. I don’t care if you put a life jacket on, you get on the shallow end, and then you just walk the distance of the pool. It’s good exercise and I encourage you to do that.

Two more quick thoughts: It saddens me that a lot of doctors and patients alike don’t know the following fact - smoking cigarettes speeds up MS.  Let me say that again that a patient with MS who smokes cigarettes is more likely to have a more rapid disease course than a patient with MS who doesn’t. Often times, I have a patient that subjects himself to a shot a day or a shot a couple of days a week and simultaneously with the same hand they’re smoking cigarettes and spitting up their disease.  Now, you’re an adult and you’re going to make your own decisions, but I really want you to know that.  I also want you to know that smoking cigarettes increases your risks to get MS.  If your child is smoking then take that very seriously because they already have a parent with MS, which puts them at high risk in the general population, and now their smoking cigarettes which increases their risk further.  You can draw your own conclusions.

Thank you very, very much for giving me the time to talk with you tonight. I really think it’s an honor. I appreciate it and I dedicate it to my uncle.

Kasey Minnis: Dr. Boster, thank you so much! We really appreciate you being here with us tonight and taking the time. What an informative presentation. I look forward to hearing your next presentation and I thank you so much for being here.

Dr. Boster:  Have a very good night.

Kasey Minnis:  On behalf of the foundation, I’d also like to thank all of our attendees. We’re glad that you joined us. There will be an audio copy of this presentation made available on the MSF website within the next week. That website is www.msfocus.org. Finally, I’d like to let you know that this program was sponsored by an educational grant from Teva Neuroscience and extend our thanks to them for their support. Thank you all and good night!

 

 



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