transient

I can't figure out whether to laugh and hate myself or call the authorities. IMO, it seems more like Bill O'Reilly.

While he never would have gotten it done without the cast around him, that was the K-gun in a nutshell. Marchibroda's "genius" was in seeing that he had one of the few true field generals in the game and some of the best talent in the game surrounding him. Give Kelly a handful of basic plays that he could run out of any formation and let him call them at the line based on the defensive alignment and his absolutely unparalleled feel for the game. Kelly's go for the throat style was perfect for keeping defenses on their heels. Put Marino in that offense and he'd have wasted it by throwing 60 times per game with his ego, but Kelly kept things balanced cuz all he wanted to do was win, and if you didn't want it as badly as he did, you'd better get used to his teeth in your ass. Give Marchibroda credit for recognizing what he had. Personally, I have always felt that beloved Marv is largely to blame for those SB losses. While the Bills were clearly the class of the AFC those years, the NFC was churning out some monsters. Levy always stuck by the mantra that the teams that execute best win games, which really missed the point that they were up against comparable if not better teams; meanwhile Parcells, Gibbs, and Johnson were putting together something new cuz they realized they were up against a comparable team talent and execution-wise. Not the best idea to go up against big game coaches without anything new up your sleeve. Sorry... I'm not much on letting old wounds heal.

Depends on what he thought of his coverage skills.

Kilpatrick was ousted from office two years ago (at least) in a sex/misappropriation of funds scandal. IIRC he did prison time for it. Just Wiki'd him, and he's back in prison for violating his parole, and has federal charges against him stemming from his time in office. The truth is, he ran the city like a mob boss, and his whole administration reeked of corruption.

I'll admit I don't know much about Allen, so I'll take your word for it. This situation or a combined GM/HC roll is the only way coaches like Shanahan or Cowher would agree to coach an organization at this point in their careers IMO. Personally, I have no ill will against Shanahan, and actually don't think he would have been a good fit. From a personnel perspective he seemed to bring in players by the truckload in FA, and if they didn't pan out he'd take the cap hit and find another, something I don't see playing well with Ralph (however, fits right in with Washington's MO under Snyder).

I agree. The Bills may have stumbled on the right person in spite of themselves, similar to promoting Polian to GM from the scouting ranks. The thing that could be really beneficial is if Whaley turns out to be legit, cuz he's essentailly a GM in training, which smacks of Nix wanting to stick with this as long as it takes to turn it around and achieve his goals (SB hopefully) and turn the reigns over to a handpicked successor. Tell me that wouldn't be a legacy. And while it may not have been the sexiest pick, the early signs philosophically are that Gailey may have been the right person to coach this team (though the season will obviously be much more telling.) IMO as soon as a GM was hired it was an indication that we would not get one of the big names, especially if the GM had a pair of stones and a vision for the team. We'll see how the power struggle develops in DC between Allen and Shanahan.

Did you then feel bad about yourself... like after watching Bad Santa? Or did you laugh some more, and then work on your kid's reaction time? I'm actually surprised that no one has pointed out that Trent's actually very adept at keying in on a single target with heightened anticipation, and therefore it's not surprising that he was good at this gimmick.

Didn't you get the point? No shouting... especially that. I mean, there was a thread aimed at banning "Shout" the song the other day. Take the hint. If you want to be demonstrative about something insult another poster's intelligence, or manhood, or mother, or something... add fifty or sixty swearing icons or head bashes, cuz they're not nearly the punch in the eye that capital letters are. Anyway, welcome aboard and go bills!

I'd vote for a likeness of Mekhi Phifer painted by Picasso. FWIW, I like Lynch the running back and what he brings, but I think last year he tried to bulk up prior to the season IIRC and he just didn't look as quick to me. Don't know if that's cuz he never adjusted to the weight, or cuz he missed the first 4 games and never got back into the swing. I see our trio this year with FJ and ML as the mainstays in the backfield with CS all over the place in specific situations. As far as Lynch the person, meh. He's not the most reprehensible player in the league, but he does strike me as an immature knucklehead who'll be out of a job if he doesn't grow up.

I've always lumped him and Brad Johnson in a similar category, though I think Johnson threw the ball more. Decent arms, good decision makers, good game managers, give you what you need without a lot of flash therefore not in the highlight reels enough for the ESPN watching world to fall in love with them.

Not only that, but IIRC they fell in love with his arm the last 8 games of his first season and completely abandoned the running game, thereby making him more of a sitting duck and exposing his weaknesses. Not that he wasn't tearing it up the first 8, but they didn't even try to keep the defense honest the last 8. Wonder if that was his quest for stats, or bad OC, or both.

Given their research interests, I think Bailes and Omalu requested to do the analysis, and the ME deferred. Can't prove it, but that is my gut feeling. I was scanning Omalu's papers (which BTW Bailes is also an author on... didn't realize it when I posted before), and got the impression that 2 of the 5 cases were conducted in a similar way - gross exam, formalin fix whole brain and send to them. Two underwent a fresh brain cutting and histologic exam as well, and random blocks were sent to them, and one had nothing other than a gross exam, return to the cranial vault, and nothing more until tissue was requested by them. Given that Henry's death was high profile, I'm sure someone affiliated with Bailes and Omalu was on the phone about the possibility of getting involved in the process as early as possible. Again, gut feeling. It also explains Henry's mother's involvement. I don't envision his mother thinking "He jumped off a truck and died so maybe he had brain damage and I should hire the world's foremost expert to prove this so I can sue the NFL" as a more likely scenario than Bailes and Omalu contacting her to ask to examine her son's brain for research, especially given the relative rarity of NFL players. She'd have to give consent both to the exam and to the release of findings at the press conference. Unless I'm missing something where she referenced possibly suing the NFL... I've only been looking at the links posted in this thread regarding her involvement.

AND coach them right. The first part is easy.

www.health.wvu.edu/services/spine-center/pdf/bailes.pdf (copy and paste to browser, I can't get it to work as a hyperlink) http://neoforenxis.com/index.php?option=co...1&Itemid=41 Here are the CVs of Bailes and Omalu. Omalu is boarded in both forensic and neuropathology. Between the two they've had close to 500 publications, speaking engagments, etc, and have been grant funded in the range of 27,000,000 dollars. They are heavily involved in the study of head injuries and their long term effects in the NFL and other sports (HS, college, and pros), and have been concentrating on it for the past 3-4 years or more. Bailes is on the NFL advisory panel for head injuries. Omalu is the neuropathologist who described the findings of CTE in other deceased NFL players (by the description in his papers, sounds like a case report on Andre Waters, and a case series with 4-5 other former NFL players.) They have close ties to the NFL, thus their involvement. Essentially these are two of THE experts in the field of sports related head injuries. The article Doc refers to states the ME report was preliminary. The ME essentially deferred to someone who is much more qualified to look at the brain (not that the ME was not qualified, just that these two are experts in the field). I wouldn't be surprised if they contacted the ME and requested to do the tissue analysis. It decreases the chance of something being done incorrectly and invalidating any further analysis they might want to do.

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.

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.

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).

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.

WEO, all of the causes of encephalopathy you listed above cause dysfunction in the brain, and you happened to select those that are reversible to attempt to prove your point. If you were to biopsy a person's brain that was acutely encephalopathic in any one of those conditions you would find acute changes be they metabolic, inflammatory, edematous, etc if you were looking in the right place. If you WERE to biopsy them, you would ALSO get sued for malpractice, as they are all treatable conditions with a reversible cause. To suggest they universally leave no residual brain damage is also incorrect, as evidenced by the fact that people with meningitis have an increased tendency to have seizures as well as hearing deficits, especially if they had this at a young age. Regardless, I am not disagreeing with the treatable or generally reversible nature of the examples you provided. To suggest that they represent the majority of the causes of encephalopathy is wrong. They are some of the more common causes, however there are countless genetic causes that result in accumulated changes in the brain over time that can occur in people who are apparently of normal intelligence and functioning at birth and into their adult lives; there are conditions that are as a result of improper proteins within the brain; there are conditions that strip the coating off of nerves, as well as infections that can do the same that are not treatable; there are changes due to hypertension that are not necessarily acutely symptomatic, but that can be seen on an MRI... I could go on endlessly. The fact is, you mention acute causes of encephalopathy and state these are the majority, but there are numerous causes of progressive encephalopathy (slow onset changes to the brain that accumulate over time), of which traumatic encephalopathy is one. In my initial post, my statement was that Henry was awfully young to have those findings, and that I didn't think 4-5 years in the NFL would cause that. This was meant more as an "I wonder what happened to this guy earlier in his life before he became a pro football player" kind of statement. For all we know he and his delinquent friends donned baseball helmets and hit one another in the head with a bat after school from the time they were 12. Also, everyone's biology is different. He could have an underlying predisposition to a degenerative disease such as frontotemporal dementia that usually presents in a person's 50s, and similarly results in people becoming disinhibited and exhibiting poor judgement, and his chosen profession hastened it's progression by causing trauma in areas that were already susceptible thereby exacerbating it. Who knows. The fact is if other players want to use this as an excuse someone would have to biopsy their brain to conclusively demonstrate evidence of disease, something I doubt many players would be excited to have done. The thing is it's not a stretch, as several have mentioned, to think that in a population of people who have spent their lives running into things at full speed that this condition would be more prevalent. It's also not hard to believe that a sport like football would have a higher number of naturally aggressive, disinhibited a-holes succeeding given the very nature of the sport. Calling BS on Henry's mother's motive for doing this is different than calling BS on the fact that there was evidence of an underlying condition. Was it severe enough to affect Henry's decision making? Who knows, but the presence of it certainly didn't make him a more rational, thoughtful person.

Don't confuse someone being encephalopathic (exhibiting confusion or "global brain dysfunction") with the underlying etiology (or encephalopathy). You can have early stages of an encephalopathy without being frankly encephalopathic. You can't tell by biopsy or autopsy if a person was exhibiting symptoms, but in specific conditions where structural changes are present such as traumatic encephalopathy you can certainly tell if they had underlying evidence of the condition. And for the record, the "E" is for encephalopathY not encephalopathIC, as in a pathology (disease, condition, or abnormality) of the encephalon (brain). If a person was in the early stages of Mad Cow and got hit by a bus, it would not change the fact that they had the pathologic condition, even if they were not yet encephalopathic.

Agreed. I was trying to use the more common condition of a stroke to demonstrate how an injury to an area of the brain can affect well established brain functionality.

Mom better be cautious, lest they find she or pops shook him a little too hard as a kid.

Encephalopathy is not soley a clinical diagnosis, it can be made on the basis of imaging or on tissue obtained from a biopsy or autopsy as well (think of bovine spongiform encephalopathy or "Mad Cow disease"), therefore it can be made on a dead person. In terms of chronic changes, it could be seen if the person suffered repeated injury during his early years and sufficient time had passed. As I had said earlier, if the changes they saw were frontal in nature, it is not a giant leap at all to say that a person would be likely to have poor executive functioning, impulsivity, and other mood or behavioral problems that could lead to them taking risks that a normal person would not. The front part of the brain is responsible for these functions. It's the same as a person with a stroke in the left side of the brain losing the function of the right side of their body.

Not to mention that much of it is new. Think of LaFontaine in 96-97 and how new the idea of post-concussion syndrome was. Prior to that it was common for players with a mild concussion to go right back into the game, or sit out for the rest of the game before playing the next night. IIRC, Jim Kelly threw a TD in his last game that he doesn't remember. The fact of the matter is science is only starting to catch up. It's hard for players to understand the potential consequences of their decisions to play injured or hide head injuries when science and medicine are only now starting to uncover their true impact (no pun intended). Imagine trying to comprehend as a football player that even if you don't have obvious evidence of a concussion, the simple fact that you continually run in to things as part of your job will most likely impact your brain function later in life. Soldiers who have been in the vicinity of large explosions without any obvious physical trauma are now showing signs of traumatic brain injury due to the concussive waves. We've got a lot to learn.

From a pathology perspective they should be able to see both acute and chronic changes and sort them out. The chronic changes are essentially a form of scarring that occurs slowly and gradually, or deposits in brain tissue that are not normally seen until later in life, and would not be related to or even expected from the acute trauma. If the damage is widespread, or is significant in the front parts of the brain, the effect can be increased impulsivity, poor decision making or "executive function," or a whole host of mood related and behavior related problems. I'm not so much calling BS as I am wondering what was going on to cause this in his brain at such an early age. 4-5 years in the NFL probably wouldn't cause these changes to show up prominently at this point in time.