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Chronic Traumatic Encephalopathy in the NFL_Robert Cantu

Chronic Traumatic Encephalopathy in the NFL_Robert Cantu -...

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Unformatted text preview: Robert C. Cantu, MD. Eepecmem of Surgeon 8m: ’1, Massachusetts i‘lEURflfiURGEfi‘! CHRONiC TRAUMATtC ENCEPHALOPATHY in THE NATIONAL FOOTBALL LEAGUE "'“ www.morosurgery—oniinelcom "‘ '5' 1:33.722 7‘33 .NEEfiCdflaopoi 43336391} Neurosurgery 6 F 225425 min. hen Andre Waters, a hard hitting National Footbaii League {NFL} safety from £984 to 1995, made the front page of the New York Times on Yoursday, January 15, 2007, he became the third NH. piayer known to have died as a result of chronic traumatic encephalopathy (GTE) attributed to the multipie concussions he expe- rienced while piaying in the NFL. Preceding the 44-year-old Andre were Mike Webster, age 50, the Hali of Fame Pittsburgh Steelers center who died homeless, and Terry Long, ago 42, who, like Waters, took his own iife {6, 7}. All three of these athletes were icnown as iron men, hard hitters who never came out oi the game, continuing to play through countless injuries, inciuding concussions, Ail of these athletes, as "weli as Ted johnson, Whose front- page story was wideiy circulated February 2, 2007 in the New York Times and Boston Globe, shared symptoms of sharply deteriorated cog- nitive function, especially recent memory ioss and psychiatric symptoms such as paranoia, panic attacks, and major depression after mul— tiple concussions experienced in the NFL. The brains of all of these deceased athietes were examined by Bennett Omalu, Mil, a forensic pathologist at the University of Pittsburgh, and shared common features of GTE including neurofibrillary tangies, new trophii threads, and celi dropout He iikened Waters’ brain to that of an “octogenarian Alzheimer’s patient.” ARE THE FlNDiNGS OF CTE EN THE BRAiNS OF WEBSTER, LONG, AND WATERS A SURPRISE? Certainly the Waters finding was no sur- prise to Iutian Bailes, Mil, medicai director, and Kevin Gusidewicz, Phil}, the Director of the Study of Retired Athletes at the Uni- versity of North Carolina at Chapel Hill. Their study of retired NFL piayers pubiished in this journal found that those who had sus- tained three or more concussions were three times more likely to experience "significant memory probiems” and five times more likely to develop earlier onset of Aizheimer’s disease (3} A study pubiished this year by the same authors found a similar reiationship between three or more concussions and clin- ical depression (4). The NFL’s own publications in this journal on concussion state that they had Seen no cases of CH". in the NFL (8—10). 'i‘hat finding is not a surprise as the NFL study inciuded oniy active players in their 205 and 395 during a short 6—year window from 1996 to 2001. Other significant iimitations of the NFL stud ies include the foilowing: 1) History of concussion: previous concussions either in the NYSE in the years before the study began or during their playing careers in high school, coilege, or other levels of football Were not included. 2) The popuiation of NFL piayers changes from year to year: new piayers enter the ieague, older players leave the league, and we do not know the number of players who constituted the 1995 population who are stili in the league in subsequent years. 3) There was difficuity coliecting data on loss of consciousness; the initiai data collection sheet did not ask for data regarding loss of consciousness. 4} This was a multisite study with numerous different examiners; there was no uniform method of evaluation of concussion in this study. 5) Return to piay data were coliected on play- ers with initiai and repeat concussion: there are many other factors that go into the deci— sion of whether or not the piayer shouid return to play, inciuding the importance of the player to the team; the importance of the upcoming game to the team; and pres- sure from owners, piayers, and their fami- lies, coaches, agents, and media may cer- tainiy influence the final decision on when the player returns to play. VOLUME s1 E NUMBER 2 I aucusmoor l ears m’aNWNNN’Manww-rwuN‘u‘w‘mw """WMWN xwwmwmlzw wva rims >1 w w wavww u i“ { .4 i E s, t a a f r Q CA:er 6) The results apply to NFbievel players: extrapola- tion to younger players has been demonstrated, Should we be surprised that CITE has been reported in for- mer NFL football ptayers? i would echo Dr, Bailes and say “absolutely not," but for additional reasons. Before lenumer- ate, let us first go back to the definition or” CTE. GTE, or dementia pugiiistica, was first described by Harrison 5. Martland in his landmark fournai of the American Medical article published in 1928 {5} as being characteristic rissocirzn of boxers “who take considerable head punishment seeking so "common in second only to land a knockout blow.” it was a} rate fighters used for traintng purposes." The early symptoms he described were a "slight mental confusion, a general sloww oh, and tremors of log in muscular movement, hesitancy in spec the hands!” Later, marked truncal ataxia, Parkinsonian syn- drome, and marked mental deterioration may set to, "necessi- tating commitment to an asylum” (S, p 3183). Although Martiand first described the clinical syndrome of CTE and Roberts (21) echoed the dangers of chronic brain dam- ages in boxers in 1969, it was Corseliis et at. who first identified the neuropathology of this syndrome in the brains of 15 deceased boxers, eight of whom were either world or national champions (1). Table 2 summarizes his findings of the four main components of this entity, areas of the brain damaged, and resultant signs and symptoms. it is critical to understand that although Corsellis pointed out four different areas of the brain and the resultant signs and symptoms, he did not state that all four areas needed to be involved for the diagnosis to be made. In fact, only eight out of 15 brains studied had all four areas of pathology present (2}. it was Corsellis who also reported CTR not only in boxers but other sports with a high risk of head injury, including those in which head injury occurred in declining frequency; among these were iockeys (especially steeplechasers), professional wrestlers, parachutists, and even a case of battered wife syn- drome. With this history, it is no surprise to have cases from NFL football. TABLE 7. Four main components of chronic brain damage in dementia pugilistica Area damaged adjacent Altered affect (euphoria, emotional ability) and mommy Parkinson’s syndrome of tremor, :igldlty, and brachykinesia Clinical symptomsr’signs Septum pellocldom, periventrlcular grey matter, frontal and temporal lobes Degeneration of the substantia nigra Cerebellar scarring and nerve cell loss Oéttuse neuronal loss Slurred speech, loss of balance and coordination loss of intellect, Alzheimer’s syndrome 334 ; VOLUMEb’i [ NUMBERE | suousraow SO WHAT ARE THE QUESTIONS TO BE ANSWERED? The most pressing question to be answered concerns the prevalence of the problem, The Waters case came to tight only because of Chris Nowinski, a former Aliwivy defensive tackle at Harvard and World Wrestling Entertainment professional wrestler who, after being forced to retire because of repeated concussions and postconcussion syndrome, researched and wrote a book on the subject of athletic concussions, Hearing of. Waters“ Suicide and suspecting CTE, Nowinski convinced the Waters family to send a portion of Waters' brain to Dr Ornalu for neuropathologicai examination. Since the Ted fohnson publicity in which this former New England Rattlers star middle linebacker said, “I don’t want anyone to end up like me,” I have personally examined and spoken with a number of retired NEL players with postconcus- $01“:me symptoms. Only an immediate prospective study Will determine the true incidence of this problem. Although this study could be funded by the NFL charities, the NFL should refrain from introducing potential bias with regard to the team of neurosurgeons, neurologists, neuropsychiatrists, and neuropathoiogists with athletic head injury expertise cho« sen to carry out the study. I also commend the fact that the brains of Webster, Long, and Waters have now been examined by other neuropathoio- gists who concur with Ornalu’s findings. Obtaining second opinions on such a high profile issue is just common sense. Finally, it is clear that not all players with long concussion histories have met premature and horrific ends to their lives. However, as the list of NFL players retired as a result of post- concussion symptoms (e.g., Harry Carson, Al Toon, Merrill Hodge, Troy Aikman, Steve Young, Ted lohnson, Wayne Chrebet) grows and as the number of documented CTEI cases increases, I believe the time for independent study of the prob— lem as well as NFL recognition that there is a problem is now. Recognizing that soldiers Were having problems with blast- related closed head injury, I haVe been a part of a team con» vened by the Department of Detense to write management algorittuns and protocols in the past year. I believe the NFL would be prudent to assemble such an independent impecca— bly qualified "dream team” to tackle their problem with con« cussion and resultant CTE head on. just as the National Association for Stock Car Auto Racing recently faced a prob lem, solved it, and became even more popular, I believe the NFL will lift this dark cloud if they confront the problem directly and honestly. REFERENCES 1. Corsellis IA, Burton C], Freemanvfirmme D21'he aftermath of boxing. E’sychoi Med 3:2?9—303, 197'3. 2. Corscllis IA: Brain damage in sport Lancet 1401402, 1976. 3. Guskiewicz KM, Marshall SW, Baiies }, McCrea M, Cantu RC, Randolph C, Jordan ED: Association betwaen recurrent concussion and late-life cog'nb tive impairment in retired professional football players. Neurosurgery 57:?194'26, 2005. wwwineurnsurgem-onllnemom w, v: w u .w, a saws « vw-mmnwmn Nmmwmnmwwwmnwmmmv-wwmwwxmw-nnm-uw-wmeu-uws-uwww-w- - ‘ '.’”.’H¥\H.’ «iwiwwmmswww .. n, , W ” WWW Wywwwxmum “may it WWW“ . w\ w\ w\ w w, w\ w\ MW at x a KKK—,4, 5m in CHRO CTRAUMATEC ENCE?HALOPATHY !N THE NATIONAL FoomALL LEAGUE . get-3559 3. Neurosurgery vat/mg "l, Tug; I AM: Ccncugc‘gn Anngarf 6. Nantes-agar)! )0 "Lag": x1 ‘r'i -,.-s~ .51.}3MA 31.21;»3‘i 2,” a; . ssky 5?, M szer EL, 1': MI; Hamzlmn RE, ‘z‘ifihz CH: tic encepkafipathy a Nata-mi chuébai‘; League 3:535:83. ...3~134, 2265. '53: ST, Hamzitcn 3L, Minster EL, Kamboh .‘=’ F: encepiuchafizy in a naicéonai ;Cc?b3§£ feague DC, Casson El: Cent (ssian i: gmffisiesa. 3—234, 223156. 1an 3c Scfe Lfic Neurosurge Cat-5.29.3 EEK Wei“! CH: Chronic Ere player: Far. Neurosurgery 59:35864‘3‘92, ZCC . 3 Shah: Ah , VOLUME 51 NUMBERE I AUCUSTECG? 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