transient
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Posts posted by transient
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Dilfer deserves a lot more credit than he gets. He won 19 (+/-1) consecutive games as a starter. When he took the starting job for the Ravens they were floundering without much hope for the playoffs. He came in, they won out, and then blew through everyone in the playoffs. Then they jettisoned him for a guy who looked good on the stat sheet. How did that work out again?
No he wasn't a Tom Brady or Peyton Manning type who's going to go out and put up 300 yds and 3 tds on a consistent basis, but he's a smart guy who had a good enough arm to keep the defense honest, could make just enough plays when they were needed, and didn't make the stupid mistakes that cost teams games. In other words, he was the perfect fit for that team.
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.
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Bledsoe is easily the best of the last decade. He was a guy that if you gave him protection and targets he'll find the open guy and deliver, and he'll keep the D honest with one of the best deep balls in the league, which he did his first season with the Bills. Then, not only did they let the line diminish, they let his targets go, and stood there dumbfounded when he didn't deliver. Even with that he was still the guy at the helm the last time the Bills had a winning season.
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.
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Thanks, transient. I stand corrected on Omalu's bona fides. It still begs the question as to why the ME would not do a standard microscopic examination of the organ listed as the injury cause of death. Why would they think to send this brain to WV if the cause of death was so obvious that it didn't require routine exam by the ME? Was the ME thinking of CTE? Why?
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.
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The only way you find out about young players is to let them play.
AND coach them right. The first part is easy.
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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.
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.
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.
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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.
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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.
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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).
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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.
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Encephalopathy caused by infection, liver failure, kidney failure are fully reversable in most cases and therefore will leave no pathologic damage to the brain. These are toxin related diseases.
Wernicke's encepaholpathy is caused by thiamine deficiency and when presenting acutely and treated appropriately, is completely reversible and will leave no mark on the brain.
In fact most etiologies of encepahlopathy diagnosed and treated early will have the same outcome, with no "brain damage". I don't disagree that any etiology left untreated will leave pathologic evidence in the brain and be irreversible.
However, Henry was a young guy with very low miles on him and NO history of head injury or concussion in college or the pros (he was hardly ever on the field!). And it was certainly not "encephalopathy" that made him jump on the truck. And if that is the case--what is the point of these two docs coming forth with their "diagnosis"? I'm assuming the family brought them in for a reason. "Doctor, is this an injured brain?". "Oh yes, yes it is. Let's announce this att a press conference." If you want a certain dagnosis, you go to a certain doctor. Happens a lot in medicine, doc.
Check out the doc's theory of how Henry may have developed such an advanced state of the disease which left permanent pathologic changes to his brain, despite no history of head trauma. If Henry got it that way, then every player's got it, I guess. Ditto anyone who rides a cab in Manhattan.
Transient<
I will concede that the most rare of all human diseases may have already caused brain injury well before the patient is symptomatic, but as above, nearly all other causes are overtly symptomatic and the permanent damage (pathological change) is a later sequela of the disease.
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.
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Wow....
Anyway, Yes, it is. It's a clinical syndrome and has many causes. One is brain injury. A pathology slide will not tell you if a patient was encephalopathic at the time of death--or at any time. "Mad cow" or BSE is described on pathology--the "E" because the individual was actually enchepalopathic. Hence the name.
Come on doc, you must have been present for part of med school and residency. It's hard to believe you're arguing this one. Wait--no it's not!
By the way--you're the one who jumped in on the "ACL injury".
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.
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Well stated, although encephalopathy leading to poor impulse control is a little more esoteric than a stroke. However it cannot be excluded as a major cause, especially when there's histologic evidence of it.
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.
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That was NOT the case's coroner's report. It was an opinion of a neurosurgeon and a pathologist who was asked to review the slides by Henry's mother. In fact these docs, who are completely uninvovled with Henry's care, made this announcement with her at their sides.
You see where this is going? Be skeptical.
Mom better be cautious, lest they find she or pops shook him a little too hard as a kid.
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Encepahlopathy is a clinical diagnosis--it therefore cannot be made on a dead person. Seeing chronic changes of repeated head trauma on a 26 year old is dubious. Making the link to his behavior that fateful day requires a quantum leap of faith---even on the doc who is making this claim.
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.
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Choosing to ignore evidence isn't the same as evidence not existing.
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.
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Henry take a lot of head shots?? Any concussions? You're right--he was only 26.
Hard to imagine the subtle changes in the brain morphology associated with this disease would be detectable after the guy suffers an acute, massive, fatal brain injury. And to suggest that this is why he jumped on the truck?
I'm calling a bit of bullsh*t on this report.
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.
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The long-term impact of guys taking hard hits is sadly not well understood.
The thing is, Henry was only 26. What they're describing is normally a longterm consequence of repeated head trauma. Think Mohammed Ali who has what was previously referred to as dementia pugilistica. The onset was while he was boxing, but the full effects were long after his career was over. Makes me wonder if Henry didn't experience repeated head trauma as a child or have some early form of underlying genetic or other neurodegenerative disease.
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Pretty much. 2006 was the first and high point of the Dick Levy era, which is a bit of a stick-in-eye to the Losman haters. The Bills played the toughest schedule (2.9 SOS), finished with the best combined offensive and defensive rank (pts), finished the season 5-4 with 3 of those losses by an average of less than 2 points. From there it was all downhill. (Makes the "stay the course" comment by Marv seem all the more laughable.) The second season featured a 2-5 run to the bus and by far their worst point differential (-102). Losman not only didn't continue to improve, he lost his grip on the job. The third season was the free fall year (2-9 run to the bus) when the bottom dropped out after a quick start "earned" Dick an extension against a truly weak schedule and featured more QB carousel with Edwards not being able to stay on the field and Losman losing his grip on simple execution of the basics. Then the fourth year was the train wreck that ended the ignominious Dick Levy era, with the bargain bin free agent QB picked up because he wasn't a threat turning into the starter, a guy off the Packers practice squad starting a game, and the guy Jauron had spent several seasons "developing" as his possible future at the #3 QB being tossed into mid-season retirement.
The most telling thing for me for both Losman and Edwards is the fact that they had a modest degree of early success followed by a precipitous downturn with the common denominator being coaching. Neither one may have the talent to be a ProBowl QB, but we were certainly never going to find out with DJ at the helm.
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if you dont have faith that the bills will be good every season then you love terrorists
I have a little gray terrorist that I love... wait... no, that's a terrier. My mistake.
Just what do these terrorists look like? Are there any girls in this gaggle of terrorists, and if so are we talking physical love, or emotional love?
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I'm thinking in the 6-8 win range, realistically, with the wins backloaded as this team gains some experience and the schemes start to make sense to them. The OL looked bad last year... everyone knows that, but come on, the offense looked like it was designed by Rainman.
"No, no, no. I don't want anything complicated... definitely not anything complicated. There are five offensive linemen. Six if you count the tight end. Seven if you go double tight. Yeah, definitely seven offensive linemen. Let's make the quarterback coach the offensive coordinator. Uh-oh, only six offensive linemen cuz I cut the left tackle. Uh-oh, now we gotta use Karl Malone's son who's only played organized football for three weeks. I'm going to Kmart to buy underwear, then watch Wapner."
How can the offense NOT be better. And even if they're not statistically better, nothing could be more painful than watching that ill conceived atrocity from last year. NOTHING. EVER. And even if the defense gives up an average of 150 yards rushing per game, it will still be an improvement over last season.
This season will be entertaining to me if there are signs of life by mid season and some of the young guys start to produce. Better yet, the current coaching staff is not wedded to old regime players so the best should play. As Gailey's been saying, the roster will sort itself out. As long as the trajectory is clearly upward, things are better.
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look if you want to be needlessly argumentative and dense, you've succeeded. What you haven't done is provide any reason why the person running the draft shouldn't be held responsible for the results. Tom Modrak is regularly cited as the architect of Bills drafts since 2002. Was he overuled from time to time? Sure. But to be so dense as to absolve him of primary responsibility for this roster makes no sense. If you want to defend failure, be my guest, but I am going to hold the person responsible for he draft responsible for the draft and not brainstorm reasons why it was everyone else's fault except for the guy who's been there throughout.
Modrak may ultimately end up getting the ax. Firing him this offseason would have been difficult considering Nix had to get a coaching staff together, and then sit down and evaluate the team's needs with Gailey after he was hired, leaving little time to reorganize the scouting department and comprehensively plan for the draft.
At this juncture I'm willing to give Nix the benefit of the doubt as a talent evaluator. I'm sure he trusts his own instincts, thereby reducing the weight of Modrak's input already. Based on their recent approach, I and numerous others on TSW are of the belief that Nix thinks there is more talent on this team than what the woeful coaching staff was able to showcase. If this is true AND your argument is correct (which, for the record I do not believe to be the case), then Nix firing Modrak makes even less sense, since he would have been the person responsible for acquiring that talent. Wouldn't it make more sense to wait and see if the young players develop with better coaching or are actual busts before firing the person responsible for bringing them in?
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"Modrak, the Bills' vice president of college scouting, has overseen the last seven Bills drafts."
How Do you know Fox Sports News? Were you in room when guys were drafted? What terrible reporting. They base their conclusions on the guy's title and specific job description as provided by the organization? Ridiculous.
Another thing that's weird is that the media always seems to interview Tom Modrak before and after the draft?
Since we have no idea what his role is, I wonder if all of these interviews are randomly assigned to people within the organization and he just keeps getting selected to do them?
Very weird.
http://www.buffalobills.com/media-lounge/v...c3-15c85f93f327
http://niagara-gazette.com/buffalo-bills/x...-draft-luncheon
http://www.wellsvilledaily.com/sports/x1804947188
Fox's article is speculative, at best. Just because they assign responsibility of prior drafts to him doesn't mean they're right. No one from the Bill's organization is even quoted in that article. The remaining articles you tagged feature him talking about the characteristics of players in the draft, albeit with less colorful language than what Dwight Adams used to ("He plays the game like his hair's on fire"). His role is presumably similar to Dwight's, unfortunately for him he's filled it during one of the most painful times in Bills recent history in terms of front office leadership and vision. Dwight scouted players, he didn't pick them. Organizing a draft board is different from deviating from it in the end.
I'm not a Modrak apologist, I just don't know how much responsibility is directly his. If he is ranking positions based on characteristics that his GM (during the years he had one) or coach are searching for, then Maybin (undersized and supposedly fast... ring any god awful Tampa-2 bells) would likely be graded higher than other DEs such as Orakpo, as an example. If he was putting together the board purely on talent regardless of system, then the responsibilty rests with him.
Also, if the team is drafting for need and reaching instead of taking the best player available or trading down for value, you can't blame him if the team selects their highest ranked prospect at said position and bypasses players he had ranked higher. If he happens to, again, have the position rank order skewed that compounds the problem and is his fault (and not the player's... can anybody say... DONTE). Unless he is the person pushing the player at that spot or ultimately making the final decision, the drafts are not "his" as FOX would indicate.
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I was younger then, but I remember seeing McKinnie on letterman/good morning america/etc.
I also remember going "who???" when the Bills drafted Williams. Then I asked my Dad "Dad, they said Williams was a tackle, I thought Bryant McKinnie was the best Tackle???"
Dad - "He is son, he is
"They were both hyped, no doubt. The fact of the matter was, picking either at four shouldn't have raised eyebrows as they were both projected as possible top 10 picks. Williams was an undeniably HUGE bust. Personally, though, I don't think McKinnie has played like what you would expect of a top 10 either, certainly not early on in his career, anyway.
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No he wasnt. That was Bryant McKinnie
I don't think there was a concensus top LT that year. Both were very hyped. Williams was the media darling, so ESPN was all over him. McKinnie was painted as a bit of a malcontent, and only furthered that impression with his holdout. While it is no contest as to which one of them was the better pick in hindsight, neither one of them has realistically lived up to their pre-draft billing or thier draft position.
M. Lynch ready to BALL in Buffalo
in The Stadium Wall Archives
Posted
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.