UPMC Physician Resources
Emerging Perspectives on Chronic Traumatic Encephalopathy and the Long Term Effects of Concussion
Dr. Julian Bailes discusses the different types of traumatic brain injuries and the long term consequences.
Upon completion of this activity, participants should be able to:
- Recognize Pathophysiology of Repetitive TBI
- Recognize the history and characteristics of CTE
- Identify strategies for CTE Mitigation
- Young JS, Hobbs JG, Bailes JE. The Impact of Traumatic Brain Injury on the Aging Brain Curr Psychiatry Rep. 2016 Sep; 18(9)81
- Hobbs JG, Young JS, Bailes JE. Sports-related concussions: diagnosis, complications, and current management strategies. Neurosurg Focus. 2016 Apr;40(4):E5
- Ban VS, Madden CJ, Bailes JE, Hunt Batjer H, Lonser RR. The science and questions surrounding chronic traumatic encephalopathy. Neurosurg Focus. 2016 Apr;40(4):E5
Dr. Bailes has reported no relevant relationships with proprietary entities producing health care goods or services.
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Release Date: 10/20/2016 | Last Modified On: 10/20/2016 | Expires: 10/20/2017
Okay, well thank you, great to be here with you all today and I really appreciate the award. There were a few years when we thought we weren't going to be getting any awards and I know Joe probably thought that, this was never for us about being anti-football or anti-sports, it was about bringing forward what we saw as the truth and today I want to kind of take you on that journey. It's my perspective, there are different perspectives, it's what I felt that we went through and what we were facing. I played football 10 years, I love the sport, it's still my favorite sport. I always say that when I go home none of my family or friends can remember my career with any specificity. My daughter who is 18 plays soccer at LSU and you know football gets singled out but soccer is very rough and if you see her come home with all the bruises and refusing to wear a dress because of all the wear and tear that her legs take you know that the brain is at risk as well.
So what was the journey of the discovery of brain injury in football? We knew that major injury could occur, we knew that concussions could occur but was there an emerging specter beyond that? And I always say that you know we are privileged to work on this organ, we are privileged to take care of patients and children and adults that have injuries to this organ, the most complicated structure on the face of the earth. The neuroscientists tell us that the brain contains, the human brain, over 100 billion neurons and if you see those connecting fibers Dr. Ogonkwo showed you very eloquently this morning our ability track those fibers and see them is for the first time really kind of a game changer. But these are the major structural pathways that we have to know where they are and what they are doing. Now you know right now you all know the pressure of the chair on your rear end, but you don't think about it until I call it into consciousness. You also know the position of your left ankle, you have to because if you stood up to leave and walk out you would fall down if you didn't. That's a constant flow of sensory information and there are other important structures. Sometimes I take out the amygdala which is some people say the seat of the soul, and that's an area that's very common in intractable epilepsy. And the amygdala is one of my favorite parts of the brain, it's always surveilling the environment for people or persons or interests, or for guys ESPN on the TV or food or something. So a very, very important organ obviously and I like to emphasize the privilege that we have to be studying it and learn about it and take care of it.
This is at a case of my using DTI to take out a brain tumor which is located here. So you see on the left side of the screen the corticospinal tract with the fibers coming down but on the right side you see this tumor and we know that those fibers have been splayed, attenuated out laterally. So I would not enter laterally, I would enter here right on the midline to take out that tumor. And then you see me sitting there operating on two video monitors and that's sort of the way we do it. And I apologize you know you have to indulge me a little bit when you come to hear a surgeon talk he always is showing one or two pictures of him operating. But that's the last one.
So for good or bad the interest, the media interest, the public interest in this issue of brain injury has just not waned at all. My wife told me recently when are you guys just going to cure the problem? You've been talking about it well over 10 years, why don't you just fix it? Well I say that's a little more and more difficult than that, dear. I don't say dear. But look the cultural interest, the drumbeat of interest, you've heard there was even a movie made, you heard that there was a White House Summit convened on it, so everybody wants to get involved. This remains one of my favorite quotes, 50 years ago by our forefather in neurological sports medicine Richard Snyder, who was the Chairman of Neurosurgery at Michigan, what he said basically I'll let you read. But he says basically there has never been a football field, there has never been a laboratory as good as a football field to study the effects of brain trauma. And in his 1967 book this was one of my favorite pictures really depicting in the 1960s chronic effects, we just didn't recognize it at the time. So here is a star player in his junior year on the left side, he had 4 concussions playing football. His personality changed, his grades suffered, he was not the same person. And on the right his senior picture, you can almost see it in his face. And there you see the error in the middle frame him sustaining one of his four concussions, head down tackling.
Now this is what I sort of look at as a timeline of the beginnings of football from its origins in rugby in around 1885 and Dr. Maroon mentioned the role of Teddy Roosevelt in really forming the NCAA in 1905 where there were 19 deaths that year in college football, there was no NFL at that time. But through the last century we've had epics of time and you see on the top, on the top the picture of the first, Mel Stevens, the first textbook of sports medicine which had a little bit about concussions, not much. Next to him is Tom Gennarelli and Tom Laffine and others really established for us what major brain injury was but you know when I was a resident training in Chicago we were taught that the brain wasn't injured with concussion, just wasn't working right. And we also knew in the 1990s, '80s and '90s that certain players were having their careers ended by concussion. As you see the picture of Troy Aikman and many others, and then of course a report of the first case of Mike Webster. What we don't want to happen is the picture on the bottom right and that is a drop of participation in sports. At Pop Warner we had a meeting this past week where we were shown recent data that shows that the number - the percentage of kids in America who are totally inactive, do no physical exercise at all of any type has risen from 12 to 18%, an alarming and very disturbing figure that we really - that's not the intent.
And here we are, that's Dr. Maroon and there is me with a 6'4" Bill Cowher with a pull on me and as I recall he said darn it or heck and some spit was flying. And I said heck, I don't know, coach. You know about this - no, the point I want to make is that this picture is a complete anachronism, what he was doing was not unusual, it was not inappropriate at the time. So whether it was a knee injury or a brain injury the coach would weigh in, that's the way it was always done. And we were doing the best we could at the time. We were trying to be conservative but we thought if a player cleared then they could go back in the same game. In fact the NFL published in 2007 that they had sent 49.6% of players who were unconscious back to the same game. I really don't think they were trying to hurt anyone, we just didn’t know the difference. We weren't aware at that time.
So as the drumbeat of media attention has proceeded so has the basic science and we know now that although I believe it's the minority of cases but in some cases there can be injury at the cellular level and the ultrastructural level. I mentioned the 100 billion neurons, it's also said there is connecting fibers, if you put them all together in your brain would equal 100,000 miles of fibers. So a lot potentially at risk for being injured and we know that that can happen.
Here is a slide from my lab where we concussed a volunteer rat one time, he's not knocked out, he just stumbles around like a football player and he lives a normal life. If you take his brain out a month later he has no hemorrhage, no stroke, no volume loss, looks normal but look at the number of torn fibers in his corticospinal tract at the brain stem level and we take out, one, one blow. So these are some of the things that have come to our attention as well as some of these diagrams you've seen before, the other mechanisms of concussion, the metabolic curve showing the perturbations in ions and neurotransmitters and lactate which almost always to normal in just a few minutes but there are a few that linger out there on that curve and that's the period of metabolic vulnerability. Others have suggested that it's really more based on cerebral blood flow but we are getting much more of a handle on understanding of the science. We've learned about the critical first week, that 92% or so of athletes with concussion resolve within the first week but that's a very critical time to understand and not to send them back in harm's way as you know. We've also learned a lot about the physics, things by biometrics and by biophysics studies that we never knew before.
Who knows who this is? And I'll give you a hint, it was right here at the University of Pittsburgh. It was the famous coach Pop Warner with his diagram single wing offense. And I get asked this question a lot and I'm sure you do as well and that is are there really more concussions or are we just diagnosing more? So I'll give you my opinion. This was one of the most lethal plays in football that Teddy Roosevelt outlawed, it's call the flying wedge where the players would lock arms and run down the field together and kill people and break their necks, amazingly. And that was one of the plays in the reformation in 1905 which was removed. So I mentioned that football evolved from its foundation in rugby, watch if we ponder are there really more concussions or we just think there are more and so are we diagnosing more, look at the style of play back in its origins and think about the style of play today.
This is Chicago versus the whole state of Michigan.
That same year that Teddy Roosevelt threatened to abolish football he came out with this Einstein, Albert Einstein deal with his iconic theory of the energy of a moving body and you know he based that on the work of physicists around the world but basically it said the energy of a moving body is equal to half the mass, so the size of the mass is important. But look what - look at the predominance, the importance of velocity in the equation, it does get multiplied by 2, it gets multiplied by its square, by itself it gets squared. It's predominant in the form of the energy of a moving body. The second thing that I believe has ironically paradoxically increased this perception or this real increase in concussions at least in football that the helmet has given those who are propensed to stick their head in there it's given them a false sense of security and it's caused them to use the head more and more into initiating contact. And when I played years ago we were taught to hit with the head and that was the style of play. I think football has to now devolve back to its origins in rugby.
Look at this play here, this was a play, I was on an NCA committee a few years ago where we used this one play to try to change one word in the 1976 spearing rule. Spearing said it's illegal to strike with the top or crown of your helmet with an intent to harm the other player. But watch how this Auburn player, number 5, number 4 has learned to aline the weight of his body and torso behind the blow and he also is headhunting and he also is launching, meaning he is leaving the ground. And this guy is clearly out on his feet, I believe was in the hospital 6 weeks. But this has spurred us to further action at the NCA level and this is an example of the reform from the NFL on down that egregious head to head hits, all those things I said, targeting, launching are now prohibited. So this is - this play was not many years ago but is an example of the revolution that we are in in changing the style of play.
So then the other epic really began when okay we know you could have a major brain injury and die, we knew that you could have concussion, we knew you could even have concussion and have your career ended; but we didn't know about the issue of long term effects. And then the research began to come out at the high school level, at the collegiate level showing that with more and more concussions you had longer symptoms, longer duration of being symptomatic and you were more susceptible to further concussions.
And then in 2005 and 2007 Kevin Guskiewicz and I and several others published these two papers. We had access through the NFL Players Association to a large database, over 3,000 former players. And basically when we looked at that at the request of the NFL PA we saw the usual hyperlipidemia and cardiac problems and joint pain and back pain but what we didn't expect was the high incidence of cognitive impairment and that's what jumped out at us. And MCI most of you know is a very important term, it means that you are not institutionalized, your wife can take care of you at home, she can take you to a cocktail party, you can have a drink and tell old football stories but in one or more domains of executive function, whether it's managing your own finances, having a part time job, being trusted to drive to the mall and back, in one or more you cannot function. 90% of MCI sufferers convert to AD, Alzheimer's within a decade. So it's a very important concept. Well we found the only risk factor, and we had Steve Marshall, he's a very good epidemiologist at UNC working on this, the only risk factor was that if they had 3 or more lost playing time concussions in the NFL. If they did they had a 5 times higher risk of having - already being diagnosed as having MCI.
Two years later we published a study looking at the same database, 3,400 players showing a triple risk of having been diagnosed or treated by a physician for depression in their retirement years. Again the only risk factor 3 or more concussions. Actually in 2000 a neurologist, Barry Jordan, and I presented to the American Academy of Neurology the preliminary findings of this database. So we were beginning to get a whiff of a new problem, that was long term affects. Well actually we already knew about it in a way because in 1929 the term dementia pugilistica, the fact that former professional boxers and we drew to know that about 20 to 25% of former pro boxers developed dementia pugilistica. It is also a term that somehow I'm pretty sure our school teachers didn't teach us but somehow we all incorporated that into our lexicon of being punch drunk. We knew what that meant. So dementia pugilistica was discovered by another medical examiner Harrison Martland in New Jersey and really was not studied until the 1950s when autopsy series were really beginning to look at it more scientifically.
So here you fast-forward several decades until the 2000s and here is Mike Webster who was to me the anchor and maybe in some ways the greatest player on the greatest team of all time. When Mike left his wife and kids and became very disorganized in his 40s, sold his 4 Super Bowl rings, lived in a truck in Wheeling, West Virginia and so forth, you probably know the story, when Mike died then he became the first publication in the modern era of CTE and named that by Bennett Omalu who resurrected that term which had been used before. So here it is, it was difficult because here is a modern beloved sport, a beloved athlete and a helmeted athlete. We didn't know that they were subjected to probably a milder form of dementia pugilistica. And here is Bennett Omalu and I, we've autopsied probably about 50 brains together and still keep getting samples, still keep learning more. But here is the question, really this repetitive nature, tens of thousands of blows to the head were football players merely boxers with helmets?
One of the great things about his discovery was that as opposed to dementia pugilistica where you have gross changes in the brain, cavum septum pellucidum, cerebellar scarring, volume loss, the brain in the CTE, and this is Mike Webster's brain, was normal. There were none of those findings and so he went the step beyond, he went to special stains for brain degeneration. You see on the left where everybody in this room's brain looks and on the right when you have tau antibody stain applied you see here these neurofibrillary tangles, these are clumps of tau inside the neurons. I look at it like sludge, it's clogging up the cells, they don't work right. You also see something else called neuritic threads which are these little wispy things, I can point out right there and these are remnants of old connecting fibers. So they don't typically have a predominance of amyloid although they do have amyloid, this is how this was first looked at as being distinct from Alzheimer's.
And so the timeline of CTE became in the early days then to be established through the case of Mike Webster and in the second case Terry Long, third case was Andre Waters who played for the Eagles, the fourth was Justin Strelzyk and the fifth Junior Seau who the NIH diagnosed a couple of years ago as having advanced CTE changes even though just like Mike Webster Junior Seau played 30 years, Mike played 27, he had no diagnosed concussions in his career. So the timeline was something like this, and that is an exposure to multiple cranial impacts where there were known concussions or just playing. We don't know the medical care, we don't know - certainly they weren't given neuro-psych tests and kept out, they were sent back into action. We don't know the recovery period, if there were any. and like most things in our health the genetics I'm sure are going to be one day we will figure out a big contribution. And then after that there is typically a latency period which lasts 6 to 12 years, that's when marriages fall apart and failed business, failed finances, then they get into depression, alcohol and substance abuse frequently and then onto either MCI, dementia and many end in suicide.
Let's look at the last interview of Mike Webster when he was about 45 years old.
So an amazing pictorial video graphic demonstration of someone at 45 who was too young to have Alzheimer's, and again became the first case. So we publisher our experience, part of it the Boston University group as a bigger experience looking at the characteristics and I also want to point out at this time that in contrast to Hollywood's depiction when those first 4 or 5 cases were shown to Dr. Maroon not only did he not obstruct it, he brought this public and he brought it to the NFL and that was a big milestone in the progression of our knowledge in CTE because we were, Bennett Omalu and I were at an impasse and that was a big, big step and Joe, we all thank you for taking that action. You are very welcome. And you see all his other background and the contributions that he has made but this stands in my mind right up at the top.
The neuropathology of CTE has been pretty much established as being distinct. Now that's a very complicated statement but I will explain it in a little more detail. The basic, the NIH said in a publication earlier this year that it's basically the accumulation of phosphorylated injured tau protein at the bottom of sulci and random. You know Alzheimer's once it begin and moves out of your medial temporal cortex it progresses in these braak and braak stages and is very uniform; CTE is sporadic, random, you could almost imagine through hits. It's also around blood vessels, I call that the stick in the Jell-O phenomenon. So you have relatively rigid arterial walls in your brain and then you have a phase contrast with a Jell-O type brain consistency and at those transition zones is where you also see tau accumulated. So this was a publication earlier this year to establish the criteria. And here is from that publication showing the phosphorylated tau in the depths of sulci is characteristic in a random pattern not seen in other types of neurodegeneration.
Here are some of our cases. This is some unique deposits of tau that you don't see in any other form of dementia in CTE. So first this is in the periventricular zone, all the brown around the fourth ventricle is tau, and this is in the back of the thalamus, the pulvinar area that you don't see any changes in Alzheimer's or other forms of dementia. So we are still learning, we still - there is a lot to understand, there is 6 isoforms of tau. We don't know who gets it and why. We don't know the genetic predisposition. We don't know the threshold for getting it. So CTE you know reminds of that quote that's attributed to Einstein and that is that's why we call it research because we don't know what we are doing. We don't have complete understanding so a lot of this work is continuing. We published this in the Journal of Neurotrauma last year looking at some of our specimens in our brain bank at the markers of endoplasmic reticulum stress as maybe being a locus of position of where this CTE change could occur.
Now saying that the pathology has not been established by a consensus group of neuropathologists and the NIH reporting that so that means we have a lot of work to do. We also have a lot of work to realize that you know there are so many factors to human behavior that you can't always ascribe it and I think Dr. Loveless said this earlier, you can't always ascribe this behavior change as serious as substance and alcohol abuse just because they played sports. And I think a case in point was the fourth case which is Justin Strelzyk and let me show you this clip of Justin Strelzyk and let me show you this clip of Justin who was a great player for the Steelers and played at main played offensive tackle, had a career ending knee injury in the 2000s and then his downward spiral began in his 30s.
So the media reported that he was burned, everyone was burned beyond recognition. We called the Medical Examiner in Buffalo and he told that in fact the media reports were wrong, he was ejected in the area of 80 yards and they recovered his body and he had his brain if we wanted to study it. So we obtained his brain with permission from his mother and he did have CTE changes but they were not replete. So can we say that CTE made him do that? It's very hard to use neuropathology to explain human behavior, it's hard to use anything to explain human behavior. We just don't know. There are many ex-athletes who have other reasons to have a meltdown beside CTE. So a case in point, a poignant case and that was actually in the movie, you probably saw. For some reason they were able to get that in the movie, that clip.
Now other aspects of CTE is that we don't know where this really lies on the spectrum of other brain degeneration diseases as you see in this Venn diagram. So there is - is certainly the possibility that you can have overlap syndromes that you can have both and so that remains to be sorted out. Here is two cases we looked at recently, both were demented former football players. On the left an NFL player, on the right a college player who played at a prominent SEC team. The NFL player was demented but his diagnosis was Alzheimer's, and the college player on the right his diagnosis was AD with you see again the periventricular tau protein.
Well this is sort of a complicated slide but it says that there may be different versions of this, there may be the usual onset of Alzheimer's around 65 where you see the big arrow, but there may be as tau protein beings to increase and leave the inter-ional cortex there may be progressive forms of CTE, there may be a continued rise and this is really AD or there may be a nonprogressive, maybe that inflammation that Dr. Maroon and Blalock reported on, maybe that inflammation quells especially if the person is removed from harms way, whether it's military exposure or sports exposure. And he mentioned in his paper done here from UPMC I think is the best and that was published a year or 2 ago and that really summarizes and puts the numbers in perspective. Look at this, only 63 football players reported, we certainly are not living in an epidemic. There are a lot of characteristics as you've heard about, whatever the number is it's important, it's important we try to figure it out. And it's important that we try to reduce the injury. And you see here the comparison on the left side of the chart with CTE and compared to other forms of dementia.
So there are many uncertainties about CTE. We have a woefully small number and we have several tens of thousands of players that are out there still alive or certainly at risk and only have 63 or so diagnosed or published anyway. We don't know the true prevalence or incidence, we don't know the neurodegeneration overlap, we don't know the confounders and we don't know the genetic predispositions or the exact pathophysiology, so a lot of uncertainties.
Now it was mentioned that 6 years ago I began to be the Medical Director for Pop Warner Football, the oldest and largest youth football league in the country, we have over 23,000 coaches, we have over 4,000 games every weekend. So we began to look, you know Pop Warner has a Super Bowl every December in Orlando at the Wide World of Sports, they have over 10,000 football players there. And we took our hidden camera and we saw players like this, and if I - he's emulating the big boys isn't he? And if I could have run like that when I was 9 believe me I would have. But our hidden camera also saw some of these plays.
So we became the first level of play and we studied this at our Pop Warner Leagues that we put sensors in helmets, we looked how many hits they got and we in 2012 eliminated those head contact drills in practice. Now our coaches are volunteer but we have a lot of spying eyes on the field with interested parents, so they pretty much have to follow all the rules. And our results as we began to reform youth football was that there were no more contact drills allowed in practice, there was only 1/3 of practice time was contact of any type and we partner with heads of football for coaching education. The Datalys Group, Tom Dompier in Indianapolis published last year the results showing that our current concussion rate in Pop Warner Football is less than 1% a year and also when we put those sensors in helmets we documented that there are less than 100, probably 50 to 60 blows to the head almost all of low velocity in a season. So we are proud that we have made reforms.
You may have heard a couple of weeks ago we had made the announcement that this season we eliminated the kickoff for lower levels of play. The kickoff is where most major injuries occur and where we worry about accumulating injury in the younger brain. So we with the first level of play this fall, now immediately after doing that we had several of our biggest leagues call and threaten to withdraw. Just showing you that you know when you try to do the right thing there is always a counter point of view. But this is some of the changes in evolution which has occurred at least in the youth football level. So this is really all about the concept of limiting exposure. If you don't know something, if I don’t' know all the carcinogens in tobacco then if somebody says I don't want to get lung cancer I say okay I don't know everything but how about not smoking, so that's limiting exposure. And this issue is really about repetitive injury, first introduced in the German literature in 1963. And that's what this is all about, this is not really about a single injury.
And look at this study I did looking at under Coach Noll who was a great coach and a hero to a lot of us, look at under the style of play in practice the numbers of estimated is we went back and interviewed the former teammates of these players, look in that chart nearly 100,000 blows to the head to Mike Webster. And look right on down the line. Look at Chris Benoit who was a WW wrestler, he was our case number 5. Look at his style of play at the age of 40, how many head contacts he had had. So I think this is part of a bygone era, I don't think anybody is getting this dose of head contact anymore nor should they. My nephew plays football at the University of Alabama and according to him and Coach Saban who I have talked to, they only have 5 contact practices the entire year now. Coach Saban talks about working on feet position and hand position, body position and fitting things. And you've heard about Dartmouth and their tackling dummy and so I think that's very progressive and I think these numbers even though they are not that long ago are going to hopefully already a thing of the past.
So this is the typical exposure curve whether it's 100 or less at youth and then it stutter steps up to 600 or 800 in high school and typically 1,000 in college, so we hope that this exposure is going to decrease. And this article Dr. Maroon mentioned he has veritable open access, you can get it off Pub Med if you want to read more about the issue of sub-concussion. And you know this is showing the draft of diffuse brain injury which is a different injury than just a focal injury. It's a kind of injury that ends up on the far right hand side of the curve, these are the worst injuries that we see in a Level I Trauma Center like I'm at or here in Pittsburgh. These are the ones that are in PVS, persistent vegetative state, they never wakeup, there is nothing we can do, there is no elevated pressure for us to treat, there is no blood clots or skull fracture to take out, they just don't wake up. Only a guy like Steven Segal can wake-up after being in a coma 8 years and kick everybody's butt on the way out of the nursing home, but otherwise never wake-up. So where does sub-concussion fit on that spectrum? Is it real? Is it an exposure phenomenon? Should know about it and I think we need to - I think we are taking it seriously. There is a lot of evidence at both the laboratory level and in human studies whether it's FMRI or DTI or autopsy or EEG that sub-concussion is a real phenomenon.
Dr. Ogonkwo mentioned this morning the work with T-807, we've done work with the group at UCLA using F18, DDNP, we've published a few months ago on the Proceedings of the National Academy of Sciences that we think they are right on the verge of being able to detect CTE-like changes, labeling this tau protein and amyloid in the brain. We've studied about 25 former military veterans or football players. And you can see here a picture there showing the correlation in the areas like the mid-brain and the amygdala with autopsy studies.
So last slide. Let's think of this positively, try to take you on our journey as we went through this progression. The specter of CTE, the specter of long term effects we need to all view that are in this field, and I assume all of you are or you wouldn't be here on a weekend. We need to work to continue to improve things. You know I said the Baby Boomers don't want to accept having their kids or grandkids play sports and end up with brain damage, so we need to figure it out. But look the players that I've shown you that most of the CTE sufferers were who played and practiced under what are now archaic protocols that no one would ever do anymore as I said, the rules changes that I've showed you in that video. We've revolutionized with the leaders at UPMC the recognition, the management, the detection with neuropsychological testing and clinical markers. We've formalized return to play protocols, we never send the player back the same day. There is a lot of advances at the point of care at the sideline and there is improved care whether it's multidisciplinary and pharmacological or nutraceutical treatment. And there's also improvement in retirement decisionmaking, I believe we have a better stance now and better ability to recommend retirement if it comes to that.
The future is exciting because there may be genetic tests, there may be biomarkers as you heard this morning, a simple blood test will tell you if you have it or not. We may use technology such as sensors for hit counts, maybe improved protective equipment. And hopefully we'll very soon getting in vivo testing in the living person to detect if they have evidence of damage. Great to be here with you, thank you very much.