wr Chris Henry - evidence of prior brain damage

[mcjeff215]

I gotta say, I don't know what you guys do for a living, but these are some interesting friggin' posts you're typing up. I've been Googling some of these terms for the past hour.

[shrader]

Why anyone would bring diabetes into this thread escapes me...

 

I brought it up simply because it is what I work with, so it was the first example that came to mind.

[stuckincincy]

I gotta say, I don't know what you guys do for a living, but these are some interesting friggin' posts you're typing up. I've been Googling some of these terms for the past hour.

 

Cincinnati Enquirer columnist Paul Daugherty chimes in:

 

http://news.cincinnati.com/article/2010062...-too-much-risk-

[Mr. WEO]

That certain types of encephalopathy can leave changes in the CNS is inarguable. And yes many are diagnosed clinically (and in Henry's case, as far as we know, there was no clinical diagnosis for his behavior). I just don't see why these 2 doctors would fabricate their findings. Perhaps the family is angling for a lawsuit against the NFL, and if they were, that will tell us more. But I don't see it, and I don't see them winning a lawsuit, if they were to bring one.

 

I already conceded the point in your first sentence. Doesn't change anything.

 

They aren't necessarily fabricating it for their conclusion to be dubious. They are given a brain, or a piece of it, that is badly damaged due to recent massive trauma. They are asked if they see evidence of "Chronic traumatic encepahlopathy", which they specialize in seeing (in their backwoods brain injury "centeer"), and they say "yes, we see this evidence on the path slides". Don't recall the actual ME making this diagnosis (how did he miss it??) on the post---or maybe he kept it a secret because the League got to him!

 

I don't see the woman winning a lawsuit either because the causality is just not there. But the goal of most malpractice suits is not to win a jury verict, but to coerce a settlement for the plaintiff.

[Ramius]

I gotta say, I don't know what you guys do for a living, but these are some interesting friggin' posts you're typing up. I've been Googling some of these terms for the past hour.

 

As someone who spent a year working in a neuroscience lab, listen to transient. He knows what he's talking about. As usual, WEO is talking out of his ass, and literally has no clue about what he's saying.

[eball]

I don't see the woman winning a lawsuit either because the causality is just not there. But the goal of most malpractice suits is not to win a jury verict, but to coerce a settlement for the plaintiff.

Spoken like someone without much experience in medical malpractice cases. Doctors win 95% of these nationwide; it's difficult if not impossible to "coerce" settlements in these actions.

[stuckincincy]

Spoken like someone without much experience in medical malpractice cases. Doctors win 95% of these nationwide; it's difficult if not impossible to "coerce" settlements in these actions.

 

Never seek medical treatment in OH...

 

http://www2.wcpo.com/dpp/news/local_news/i...roof-Physicians

[Doc]

I already conceded the point in your first sentence. Doesn't change anything.

 

They aren't necessarily fabricating it for their conclusion to be dubious. They are given a brain, or a piece of it, that is badly damaged due to recent massive trauma. They are asked if they see evidence of "Chronic traumatic encepahlopathy", which they specialize in seeing (in their backwoods brain injury "centeer"), and they say "yes, we see this evidence on the path slides". Don't recall the actual ME making this diagnosis (how did he miss it??) on the post---or maybe he kept it a secret because the League got to him!

 

I don't see the woman winning a lawsuit either because the causality is just not there. But the goal of most malpractice suits is not to win a jury verict, but to coerce a settlement for the plaintiff.

Sure it changes things. You were trying to claim that encephalopathy is strictly a clinical diagnosis. Hence the discovery of (I'm guessing astrocyte proliferation/scarring, which couldn't have happened the day he died, much less afterwards) encephalopathy by histological examination by the neurosurgeon and ME was bunk. Furthermore, they never said that his encephalopathy definitively caused Henry's behavior.

 

Now I can't speak as to the institute they run, but a quick search on neurosurgeon Julian Bailes and ME Bennet Omalu reveals that they're hardly unknowns. And the original ME would only have been looking for the most obvious cause of death, i.e. the head trauma he suffered from falling out of the truck. For example, I don't recall any histological studies done on his heart.

 

Lastly, while I agree that the majority of malpractice defendants look to coerce a settlement, this is the NFL we're talking about. They have deeper pockets than almost anyone and will NOT settle a case like this, because of the floodgates it would open.

[transient]

I already conceded the point in your first sentence. Doesn't change anything.

 

They aren't necessarily fabricating it for their conclusion to be dubious. They are given a brain, or a piece of it, that is badly damaged due to recent massive trauma. They are asked if they see evidence of "Chronic traumatic encepahlopathy", which they specialize in seeing (in their backwoods brain injury "centeer"), and they say "yes, we see this evidence on the path slides". Don't recall the actual ME making this diagnosis (how did he miss it??) on the post---or maybe he kept it a secret because the League got to him!

 

I don't see the woman winning a lawsuit either because the causality is just not there. But the goal of most malpractice suits is not to win a jury verict, but to coerce a settlement for the plaintiff.

 

The medical examiner is there to determine the immediate cause of death. You don't need to do an exhaustive microscopic exam of a brain to figure out what killed the guy after he fell of a truck and fractured his skull. You can tell that on a gross exam. Given that, any histologic exam would not have needed to be done urgently, and likely would not have been done by the ME himself, though it could have been. Also, depending on the staining they did, the processing can take some time, again, not likely to be related to cause of death so you can make the declaration of cause of death without having the results of the staining available. Most likely in this case, the doctors who you so quickly dismiss who are in charge of an institute that does research into brain injury probably asked for tissue to examine as Henry is a professional athlete who plays a violent contact sport. His mother would have had to give consent for that as next of kin, thus her involvement. The announcement was probably because they didn't expect the results they found, and before being able to do so, they again would have needed to get approval from his mother. This is currently a huge area of research. There has been nothing that I saw indicated about a lawsuit. With regard to the doctors searching until they find something, an encephalopathy is a global process, and as such any area that was not damaged by the fall would potentially have these changes them. "Normal" tissue would have been sampled as an internal control by the ME or pathologist, and if samples were requested by the doctors at the Brain Injury Research Institute, they certainly would have asked for samples that were both from the acute injury and "normal" controls. Sorting this out from the acutely injured regions is not at all difficult.

 

Finally, in response to your assertion that the conditions you identified earlier are THE ones that cause encephalopathy, they are one subset of a large group and are appropriately called toxic-metabolic encephalopathies. They are not even PRIMARY encephalopathies, meaning they are not due to changes taking place in the brain that are due to a primarily neurologic cause. They are due to transient metabolic disturbances, infections, inflammation, etc that affects global brain function. They may be the most commonly seen, but they are not a majority in terms of number of etiologies. There are a whole host of things you are discounting that ARE primary neurologic conditions that are more analogous to traumatic encephalopathy than the examples that you continue to tout. Apples and oranges. As I tried to explain before, an encephalopathy is a disease or condition that affects the brain on a grand scale, it is not the confusion that it causes in the person. It is expected to be seen throughout the brain, not focally like a tumor or metastasis as you suggested would need to be included based on my description. As for discounting the idea of hypertension causing this, there is an actual entity called hypertensive encephalopathy, AND there is also a phenomenon of brain injury seen in people with chronic hypertension that affects small blood vessels diffusely that can be seen on MRI that is technically an encephalopathy.

 

You can continue to call BS if you like, but you are wrong.

 

Edit: I guess I type slower and say things less succinctly than Doc.

[Zona]

Was just going to post about this. Combined with Gladwells article for the New Yorker last year, I am really starting to wonder about the future of this sport in it's current form. I am 47, and wonder if I have a normal life span to say 75..will there still be tackle football played???

 

Know sure as hell I am glad my son does not want to play orhanized football.

 

I have thought for years that if the league truly cared about reducing injuries, than they need to take off the pads and helmets. Play this game like rugby. The "throw the body around and make the highlight reel" mentality will be gone instantly. In this form of blocking and tackling, injuries would be less likely imo. Aussie Rules football and rugby dont wear pads. They survive ok. Players would adapt. The question is, would the fans?

[Mr. WEO]

Spoken like someone without much experience in medical malpractice cases. Doctors win 95% of these nationwide; it's difficult if not impossible to "coerce" settlements in these actions.

Thankfully, I have very little personal/professional experience with medical malpractice cases---mostly I review cases as an expert. Pointing out that most suits result in no judgement against the doc does not change the fact that the goal of most plaintiff's cases (or their lawyers) is to obtain a settlement, as opposed to going to trial. So your comment makes no sense at all. The plaintiff's bar knows the odds you are mentioning.

 

As someone who spent a year working in a neuroscience lab, listen to transient. He knows what he's talking about. As usual, WEO is talking out of his ass, and literally has no clue about what he's saying.

 

Yes, I have no clue what I am saying---that's one possiblity. Or, maybe all the big words are confusing you.

 

Transient does sound like like a very bright guy and he makes well thought out and valid points that I sometimes respectfully disagree with (I enjoy the back and forth with a well-informed poster).

 

You, on the other hand, put your level of intelligence on fabulous display each time you post.

[Mr. WEO]

Sure it changes things. You were trying to claim that encephalopathy is strictly a clinical diagnosis. Hence the discovery of (I'm guessing astrocyte proliferation/scarring, which couldn't have happened the day he died, much less afterwards) encephalopathy by histological examination by the neurosurgeon and ME was bunk. Furthermore, they never said that his encephalopathy definitively caused Henry's behavior.

 

Now I can't speak as to the institute they run, but a quick search on neurosurgeon Julian Bailes and ME Bennet Omalu reveals that they're hardly unknowns. And the original ME would only have been looking for the most obvious cause of death, i.e. the head trauma he suffered from falling out of the truck. For example, I don't recall any histological studies done on his heart.

 

Lastly, while I agree that the majority of malpractice defendants look to coerce a settlement, this is the NFL we're talking about. They have deeper pockets than almost anyone and will NOT settle a case like this, because of the floodgates it would open.

Where is the ME report that shows histopath? Maybe Julian Bales is a great neurosurgeon. If neuropathologist (is either doc one?) says there is clear histo evidence of this disease I would happy concede my skepticism.

 

 

The medical examiner is there to determine the immediate cause of death. You don't need to do an exhaustive microscopic exam of a brain to figure out what killed the guy after he fell of a truck and fractured his skull. You can tell that on a gross exam. Given that, any histologic exam would not have needed to be done urgently, and likely would not have been done by the ME himself, though it could have been. Also, depending on the staining they did, the processing can take some time, again, not likely to be related to cause of death so you can make the declaration of cause of death without having the results of the staining available. Most likely in this case, the doctors who you so quickly dismiss who are in charge of an institute that does research into brain injury probably asked for tissue to examine as Henry is a professional athlete who plays a violent contact sport. His mother would have had to give consent for that as next of kin, thus her involvement. The announcement was probably because they didn't expect the results they found, and before being able to do so, they again would have needed to get approval from his mother. This is currently a huge area of research. There has been nothing that I saw indicated about a lawsuit. With regard to the doctors searching until they find something, an encephalopathy is a global process, and as such any area that was not damaged by the fall would potentially have these changes them. "Normal" tissue would have been sampled as an internal control by the ME or pathologist, and if samples were requested by the doctors at the Brain Injury Research Institute, they certainly would have asked for samples that were both from the acute injury and "normal" controls. Sorting this out from the acutely injured regions is not at all difficult.

 

Finally, in response to your assertion that the conditions you identified earlier are THE ones that cause encephalopathy, they are one subset of a large group and are appropriately called toxic-metabolic encephalopathies. They are not even PRIMARY encephalopathies, meaning they are not due to changes taking place in the brain that are due to a primarily neurologic cause. They are due to transient metabolic disturbances, infections, inflammation, etc that affects global brain function. They may be the most commonly seen, but they are not a majority in terms of number of etiologies. There are a whole host of things you are discounting that ARE primary neurologic conditions that are more analogous to traumatic encephalopathy than the examples that you continue to tout. Apples and oranges. As I tried to explain before, an encephalopathy is a disease or condition that affects the brain on a grand scale, it is not the confusion that it causes in the person. It is expected to be seen throughout the brain, not focally like a tumor or metastasis as you suggested would need to be included based on my description. As for discounting the idea of hypertension causing this, there is an actual entity called hypertensive encephalopathy, AND there is also a phenomenon of brain injury seen in people with chronic hypertension that affects small blood vessels diffusely that can be seen on MRI that is technically an encephalopathy.

 

You can continue to call BS if you like, but you are wrong.

 

Edit: I guess I type slower and say things less succinctly than Doc.

Every post done on a patient I have seen includes a micro exam--especially on the organ that may have been involved in determining cause of death. If the ME has the same result, I don't see where he has come forward to corroborate.

 

Also, I didn't say they were "THE one's"--I said they were the most common etiologies of encepahlopathy. Genetic and other primary diseases of the brain simply do not cause the majority of brain injury or disfunction. I'm not discounting anything---the fact is that most encephalopathies are caused by treatable diseases and act upon the brain secondarily. Most are acute and reversible. Hypertensive encephalopathy is one such disease. Most commonly, chronic hypertension leads to lacunar strokes or catastrophic massive stroke. Many of the above acute diseases affect a specific area of the brain--not all are diffuse or global.

[jester43]

I am so sick of congress and doctors throwing their two cents in this. Ask any NFL football player about Brain Damage and the sport they play. they all recognize the risks and don't care.

 

Besides there isn't any concrete evidence for it anyway.

 

wow.

[transient]

Also, I didn't say they were "THE one's"--I said they were the most common etiologies of encepahlopathy. Genetic and other primary diseases of the brain simply do not cause the majority of brain injury or disfunction. I'm not discounting anything---the fact is that most encephalopathies are caused by treatable diseases and act upon the brain secondarily. Most are acute and reversible. Hypertensive encephalopathy is one such disease. Most commonly, chronic hypertension leads to lacunar strokes or catastrophic massive stroke. Many of the above acute diseases affect a specific area of the brain--not all are diffuse or global.

 

I'm not denying that the encephalopathies you are focusing on are common, and if you are looking at this purely from the standpoint of incidence then yes, you are correct. However, CTE is not common, and is not really comparable to the more common entities you are describing. CTE is a primary encephalopathy. It's effects are cummulative, and symptoms generally correlate with severity of histologic findings. To say that most encephalopathies are treatable is incorrect from an etiology standpoint, as most primary encephalopathies are not at all treatable. To say that the most common secondary encephalopathies are treatable is more accurate. It's a matter of perspective. From a pure numbers standpoint you win, but you do so by comparing things that are not really comparable. The thing is, the term encephalopathy is really broad and you are arguing it through a very narrow viewpoint, though the incidence of the limited number of conditions you are talking about may allow you to feel justified in doing so.

 

Also, to say that the above acute diseases affect only a specific area of the brain is technically wrong. Renal failure and hepatic failure, as examples, lead to systemic changes, namely an elevation in the level of waste products in the blood... blood that is flowing through the entire body and causing metabolic changes in the entire body. Certain areas of the brain are more susceptible to these toxins, and therefore become dysfunctional, however the changes induced are brain (and body) wide -- that was my point in saying that if you biopsied the brain of a patient with acute hepatic encephalopathy, for instance, that you could see changes everywhere, it doesn't mean that the symptoms were necessarily coming from the area of biopsy; and I wasn't seriously suggesting that it should be done.

 

When it comes to people being encephalopathIC, the fact is it cannot be a focal process affecting only a specific area of the brain. In general, it needs to affect BOTH hemispheres, otherwise you would not have the delirium and fluctuations in consciousness that frequently accompany it, you would lose only the focal functioning. People with acute strokes, unless they have injury in both hemispheres, rarely have an alteration in their level of consciousness (in the acute setting, not applicable after there has been swelling). That is not to say they tend to external stimuli correctly, but that they are wide awake and alert (also doesn't apply to the certain areas of the brainstem or thalamus, as this can cause signficant changes in level of consciousness).

 

Finally, with chronic hypertension there are commonly white matter changes on MRI (when severe referred to as leukoaraiosis) that frequently precede the lacunar and larger strokes you are refering to, and the condition is technically an encephalopathy (though admittedly it is currently poorly described and may turn out to be more accurately described as a vasculopathy).

[transient]

Transient does sound like like a very bright guy and he makes well thought out and valid points that I sometimes respectfully disagree with (I enjoy the back and forth with a well-informed poster).

 

Aww, shucks.

 

Right back at cha. I especially appreciate the fact that it hasn't become personal warfare littered with the annoying swearing incon or the headbashing icon.

[Doc]

Where is the ME report that shows histopath? Maybe Julian Bales is a great neurosurgeon. If neuropathologist (is either doc one?) says there is clear histo evidence of this disease I would happy concede my skepticism.

Mecklenburg County (Ohio) ME Carol Cormier did the original autopsy on Henry. I don't know her credentials. I don't know if she did histopath on any of Henry's tissues, but I don't know why she would have, given that the cause of death was obvious. If she did histopath on his brain, she might as well have done it on his heart, looking for a zebra like an MI as a result of the trauma. So just because we didn't hear about him having CTE on his original autopsy, it doesn't mean Cormier looked for it. I don't know if this is what you getting at above, but you seemed to suggest this earlier.

 

As for the docs at BIRI, they looked at histopath of Henry's brain. I don't know if either is a certified neuropathologist, but I'm sure they know what normal versus diseased brain looks like:

 

The doctors had done a microscopic tissue analysis of Henry's brain that showed he suffered from chronic traumatic encephalopathy.

 

As for their motives, it wouldn't surprise me to learn that Henry's parents are trying to use the histopath to excuse their son from his actions. I don't buy that entirely, although I doubt the CTE helped matters any. And again I also don't think they have a snowball's chance in hell of winning a lawsuit, since Henry played a lot more football before he got to the NFL, than in the NFL. Hopefully their motives are only to try and bring more attention to what can happen beyond when a player gets a concussion, something the NFL has begrudgingly started to take seriously, and not financially motivated.

[transient]

As for their motives, it wouldn't surprise me to learn that Henry's parents are trying to use the histopath to excuse their son from his actions. I don't buy that entirely, although I doubt the CTE helped matters any. And again I also don't think they have a snowball's chance in hell of winning a lawsuit, since Henry played a lot more football before he got to the NFL, than in the NFL. Hopefully their motives are only to try and bring more attention to what can happen beyond when a player gets a concussion, something the NFL has begrudgingly started to take seriously, and not financially motivated.

 

Assuming this quote from the initial article is factually correct, "Glaspy gave Bailes permission to examine her son's brain in detail," I would assume Bailes asked to examine Henry's brain due to research interests. If you google him, his CV is online, and he has an interest in cognitive deficits in retired NFL players. Not to be crass, but from his perspective NFL players are a resource to be studied, and a rare resource at that. I expect that he contacted Henry's mother, not vice-versa.

[Mr. WEO]

I'm not denying that the encephalopathies you are focusing on are common, and if you are looking at this purely from the standpoint of incidence then yes, you are correct. However, CTE is not common, and is not really comparable to the more common entities you are describing. CTE is a primary encephalopathy. It's effects are cummulative, and symptoms generally correlate with severity of histologic findings. To say that most encephalopathies are treatable is incorrect from an etiology standpoint, as most primary encephalopathies are not at all treatable. To say that the most common secondary encephalopathies are treatable is more accurate. It's a matter of perspective. From a pure numbers standpoint you win, but you do so by comparing things that are not really comparable. The thing is, the term encephalopathy is really broad and you are arguing it through a very narrow viewpoint, though the incidence of the limited number of conditions you are talking about may allow you to feel justified in doing so.

 

Also, to say that the above acute diseases affect only a specific area of the brain is technically wrong. Renal failure and hepatic failure, as examples, lead to systemic changes, namely an elevation in the level of waste products in the blood... blood that is flowing through the entire body and causing metabolic changes in the entire body. Certain areas of the brain are more susceptible to these toxins, and therefore become dysfunctional, however the changes induced are brain (and body) wide -- that was my point in saying that if you biopsied the brain of a patient with acute hepatic encephalopathy, for instance, that you could see changes everywhere, it doesn't mean that the symptoms were necessarily coming from the area of biopsy; and I wasn't seriously suggesting that it should be done.

 

When it comes to people being encephalopathIC, the fact is it cannot be a focal process affecting only a specific area of the brain. In general, it needs to affect BOTH hemispheres, otherwise you would not have the delirium and fluctuations in consciousness that frequently accompany it, you would lose only the focal functioning. People with acute strokes, unless they have injury in both hemispheres, rarely have an alteration in their level of consciousness (in the acute setting, not applicable after there has been swelling). That is not to say they tend to external stimuli correctly, but that they are wide awake and alert (also doesn't apply to the certain areas of the brainstem or thalamus, as this can cause signficant changes in level of consciousness).

 

Finally, with chronic hypertension there are commonly white matter changes on MRI (when severe referred to as leukoaraiosis) that frequently precede the lacunar and larger strokes you are refering to, and the condition is technically an encephalopathy (though admittedly it is currently poorly described and may turn out to be more accurately described as a vasculopathy).

Some acute causes affect focal areas, as doc pointed out with regard to Wernicke's.

 

Anyway, any ME who performs a cursory gross exam only on the organ that is directly involved with the presumed cause of death has not completed her autopsy and needs to get back to work. Even minimal curiosity (as well as a professional compulsionto perform an adequate postmortem) would have lead to a standard microscopic examination of the brain of a young man who just decided to jump onto a truck that was sent speeding down the road.

 

Doc, again, I don't think they could win a lawsuit. The goal would be to build a case with these world experts as witnesses and some hoped-for public sentiment about this disease to get a seetlement. The NFL has endless money for a defense, but I've seen jury verdicts that have no relation to the facts of a case. These are not juries of your peers, doc.

[Doc]

Some acute causes affect focal areas, as doc pointed out with regard to Wernicke's.

 

Anyway, any ME who performs a cursory gross exam only on the organ that is directly involved with the presumed cause of death has not completed her autopsy and needs to get back to work. Even minimal curiosity (as well as a professional compulsionto perform an adequate postmortem) would have lead to a standard microscopic examination of the brain of a young man who just decided to jump onto a truck that was sent speeding down the road.

I found this article on his autopsy:

http://news.cincinnati.com/article/2010060...after-his-death

Looks like they harvested every intact organ, thus precluding a thorough examination of his body, and were only interested in the obvious and immediate cause of death, and whether he was under the influence of just alcohol. It also looks like they punted, so to speak, on the histopath of his brain to Bailes and Omalu.

Doc, again, I don't think they could win a lawsuit. The goal would be to build a case with these world experts as witnesses and some hoped-for public sentiment about this disease to get a seetlement. The NFL has endless money for a defense, but I've seen jury verdicts that have no relation to the facts of a case. These are not juries of your peers, doc.

I don't disagree that Henry's parents might still try to bring a lawsuit, and that they could possibly win. Dumber lawsuits have been tried before. But the NFL would appeal until his parents ran out of money and/or the lawyer stops working on contingency. IOW, there's no way they would settle.

[Mr. WEO]

I found this article on his autopsy:

http://news.cincinnati.com/article/2010060...after-his-death

Looks like they harvested every intact organ, thus precluding a thorough examination of his body, and were only interested in the obvious and immediate cause of death, and whether he was under the influence of just alcohol. It also looks like they punted, so to speak, on the histopath of his brain to Bailes and Omalu.

 

I don't disagree that Henry's parents might still try to bring a lawsuit, and that they could possibly win. Dumber lawsuits have been tried before. But the NFL would appeal until his parents ran out of money and/or the lawyer stops working on contingency. IOW, there's no way they would settle.

Shoddy work. Why even do a gross organ exam? Why not just eyeball the body and sign the sheet: "massive head trauma"? To hear the WV docs, even a cursory micro exam would have revealed this CTE.

 

Aside from his injuries, including abrasions to his back, Henry was disease-free and healthy, according to the report.

 

Oops! Except for that advanced chronic brain injury!

 

Perhaps the ME summed up Henry's wasted adulthood best: “That’s a perfect organ donor,”