1
Written Testimony
Ann C. McKee, M.D.
Associate Professor of Neurology and Pathology
Boston University School of Medicine
Director of the VISN-1 Neuropathology Laboratory for the New England Veterans
Administration Medical Centers
Director of the Brain Banks for the Boston University Alzheimer’s Disease Center,
Framingham Heart Study, and Centenarian Study
Co-Director, Center for the Study of Traumatic Encephalopathy
Hearing before the House Judiciary Committee
Legal Issues Relating to Football Head Injuries
October 28, 2009
2
3
Mr. Chairman and Members of the Committee:
Thank you for the invitation to testify today on legal issues relating to football head
injuries. My name is Dr. Ann McKee. I am an associate professor of Neurology and
Pathology at Boston University School of Medicine, and I am the Director of the
Neuropathology Laboratory for the New England Veterans Administration Medical
Centers at the Bedford VA Medical Center, the Director of the Brain Banks for the
Boston University Alzheimer’s Disease Center, the Framingham Heart Study, and the
Centenarian Study, and I am a co-director for the Center for the Study of Traumatic
Encephalopathy at Boston University.
I received my medical degree in 1979, and I am board certified in both Neurology and
Neuropathology. I have extensive experience in neuropathology of neurological disease
and have written extensively on the neuropathology of many neurodegenerative
diseases, including Alzheimer’s disease, Parkinson’s disease, and Frontotemporal
Dementia, as well as normal aging. For the past 23 years, I have been studying the
brains of individuals after death and correlating the pathological findings to the patient’s
clinical symptoms during life. I have examined thousands of brains, brains from people in
all walks of life including brains from individuals who have lived to be well over the age of
100. In addition, for most of my professional career, I have been focused on tau protein,
a protein that becomes toxic when abnormally phosphorylated and builds up in the
brains of patients with some neurodegenerative diseases, including Alzheimer’s disease,
but is found only in very limited quantities in the brains of normally functioning people.
In January of 2003, as part of my work with the Boston University Alzheimer’s Disease
Center and the Bedford VA, I examined the brain of a man who died at the age of 72
after 15 years of severe dementia requiring institutionalization. The man had been a
4
world champion boxer and had been clinically diagnosed with Alzheimer’s disease
beginning at the age of 58. However, when I looked at his brain on post-mortem
examination, I found that there was absolutely no evidence of Alzheimer’s disease;
there was no evidence of beta amyloid, a protein that accumulates in the brain in people
with Alzheimer’s disease and is thought by many to be the cause of Alzheimer’s disease.
Instead, the brain of this world champion boxer showed a massive build-up of the toxic
form of tau protein as neurofibrillary tangles (NFTs) and glial tangles throughout his
brain. The neurofibrillary and glial tangles were also distributed in a unique pattern, a
pattern not found in any neurodegenerative condition except Chronic Traumatic
Encephalopathy, or CTE. In CTE, tau protein builds up in individual nerve cells and
prevents them from making normal connections with other nerve cells, eventually killing
the cells. In this man’s brain, there were massive numbers of NFTs and glial tangles, so
many in fact that you could see the abnormalities on the glass slides without the use of a
microscope, as you can see in the right panels of Figure 1. There is tremendous
accumulation of tau protein that appears as a brown pigment. All the brown pigment you
see is abnormal, please compare what you see on the right to the brain of a normal 65
year old man on the left, all the slides are prepared and stained in exactly the same way,
and there is absolutely no brown pigment visible in the normal individual. When you look
at the brain microscopically as in the lower panels, you can see that many individual
nerve cells of the boxer contain NFTs – they are found in nearly every nerve cell and
there are almost no normal appearing cells. This individual, a former professional boxer,
was clinically diagnosed with Alzheimer’s disease during life, but the disease that
actually caused his tragic 15 year decline in intellect and eventually killed him, was CTE,
a disorder that would have been entirely prevented if he hadn’t suffered repeated head
injury in his younger years as a boxer.
5
My second case of CTE came in 2004, again when I was examining the brain of a man
who had been clinically diagnosed with Alzheimer’s disease when he was alive. When I
looked at the slides, I immediately realized that the changes found in this individual were
nearly identical to those that I had found in the world champion boxer, but in this case,
the medical records did not indicate that he had ever had any head injury. So I called the
patient’s daughter, and sure enough, it turned out that the man had been a professional
boxer during his twenties. Again, his post-mortem examination indicated that his
functional deterioration, dementia and placement in a nursing home were not due to
Alzheimer’s disease, but instead due to CTE, a disorder that could have been entirely
prevented. Over the ensuing years, I examined several other cases of CTE in
professional boxers, all with a similar appearance and pattern of abnormalities.
I met Chris Nowinski in the summer of 2007 and through Chris’s efforts in early 2008, I
had my first opportunity to examine the brain of a retired professional football player. It
was the brain of John Grimsley, a former linebacker for the Houston Oilers who had died
of an accidental gunshot wound while cleaning his gun at the age of 45. According to his
wife, he was concussed 3 times during his college football years, and at least 8 times
during his NFL career, however, only one "cerebral concussion" was medically
confirmed. He was never formally diagnosed with post-concussion syndrome and never
sought medical attention for residual cognitive and behavioral difficulties. There was no
history of ever losing consciousness for more than a few seconds and he never required
being carried off the field or hospitalization. He never took any performance-enhancing
drugs or used illicit drugs. He was a nonsmoker and there was no known family history
of dementia.
6
According to his wife and close friends, he began showing changes in his behavior and
cognitive decline at age 40. He developed difficulties in short-term memory, attention,
concentration, organization, planning, problem-solving, judgment, and the ability to
juggle more than one task at a time. For example, he would ask the same questions
repeatedly over the course of the day and he would ask to rent a movie that he had
already seen. He had difficulty assembling his tax records, shopping alone, and
understanding television. His symptoms gradually progressed and became quite severe
by the end of his life. He also developed a “shorter and shorter fuse” and would become
angry and verbally aggressive over seemingly trivial issues.
When I first looked at his brain (it had been previously dissected by the coroner), I didn’t
see any gross changes. Yet when the microscopic slides were prepared, they showed
the exact same pattern of changes that I had found in the brains of the boxers with CTE.
There were large numbers of tau containing neurofibrillary tangles throughout all parts of
the brain and there was absolutely no evidence of beta amyloid protein or Alzheimer’s
disease. The brain of this 45 year old husband and father, at the prime of his life,
showed profound neurofibrillary degeneration, changes of CTE that were identical in
nature to the changes I found in the brains of the boxers, but were now in a football
linebacker some 30 years younger. In John Grimsley’s brain, there were striking
changes in regions of the brain controlling personality and behavior, such as the frontal
lobes, profound changes in the areas controlling impulsivity and rage behavior such as
the amygdala, and severe changes in anatomic structures that are responsible for
memory, such as the hippocampus, mammillary bodies and thalamus. In Figure 1, the
brain of John Grimsley is seen in the middle; in the top middle panel, you can see severe
tau deposition in the frontal lobe and microscopically; in the bottom middle panel, you
can see numerous nerve cells containing tau and NFTs.
7
Figure 1
In a normal 45 year old, absolutely none of these changes would be found. Indeed these
changes would not be found in a normal 65 year old, 85 year old or 110 year old.
8
The next football player’s brain that I examined was that of Tom McHale, a 45 year old
retired offensive lineman for the Tampa Bay Buccaneers. He was a husband and father
of 3 young boys. After a 3 year decline in his ability to make sound business decisions,
increasing apathy, depression, and memory loss, he died as a result of substance
abuse. His wife did not know of any reported formal concussions during his year as a
lineman. His brain too showed profound tau immunoreactive neurofibrillary
degeneration in areas controlling memory, impulsivity, organization and problem solving
(as you can see in Figure 2) and again with no evidence of any other disorder other than
CTE.
Figure 2
The third brain of a professional football player I examined was that of Wally Hilgenberg,
a 66 year old former linebacker who died from complications related to Amyotrophic
Lateral sclerosis or Lou Gehrigs disease. He played 16 seasons with the Minnesota
Vikings and had at least 10 concussions, including losing consciousness on 1 or 2
occasions. He began showing slow and steady cognitive decline at the age of 56. His
cognitive difficulties were manifest mainly by “not understanding things at a deeper level”
and he had difficulties with executive functioning, including worsening organization and
9
planning skills. His cognitive decline progressed with worsening memory and language
functions. In his last year, he stopped being able to read and was completely unable to
learn how to operate an assistive communication device, even using the simplest level of
commands. Inspection of his brain showed damage to the frontal cortex in a pattern that
suggested it had been used as a battering ram, and the interior spinal fluid spaces were
enlarged suggesting that the volume of the brain had declined. Microscopically the brain
was densely riddled by tau containing NFTs and glial tangles throughout the cerebral
cortex, basal ganglia, thalamus, and brainstem in the unique pattern that defines CTE,
and again, in the complete absence of Alzheimer’s disease and beta amyloid.
Furthermore, the damage found in his brain was far greater in density and the damage
was much more widespread than anything that I have ever found in Alzheimer’s disease
or any of the other common neurodegenerative disorders.
Figure 3
10
The fourth, fifth and sixth brains from former NFL football players that I examined,
including one individual who took his own life, all showed the same distinctive,
characteristic changes of CTE. The seventh brain of a former NFL player I analyzed was
that of Louis Creekmur, a former offensive lineman for the Detroit Lions and an eighttime
Pro Bowler. Louis Creekmur played ten seasons for the Lions, and was famous for
suffering at least thirteen broken noses and 16 concussions. Beginning at the age of 58,
he began to show increasing cognitive and behavioral difficulties including memory loss,
problems with attention and organization, and outbursts of anger and aggression. He
died from complications of dementia at the age of 82. The brain of Mr. Creekmur showed
extensive damage including marked shrinkage of medial temporal lobe structures that
control memory, shrinkage of the frontal and temporal lobes, and marked dilation of the
spinal fluid cavities that line the brain’s interior. There was widespread and severe tau
deposition as NFTs throughout the frontal and temporal lobes, amygdala, hippocampus,
thalamus and brainstem in the unique pattern that is only found in CTE. In Mr.
Creekmur’s case, the abnormalities were profound, they were severe, and they
paralleled the changes found in the world champion professional boxer. Mr. Creekmur
was also a member the NFL’s Plan 88. Yet again, there was absolutely no evidence of
Alzheimer’s disease or any other neurodegenerative disorder, and the findings indicated
that if Mr. Creekmur had not sustained repetitive head trauma during the play of football,
he would be alive and well and enjoying his family and grandchildren today.
11
Figure 4
I have also examined the brain of a former college football player, Mike Borich, a former
wide receiver for Snow College and Western Illinois University who died at the age of 42
after a several-year period of increasing irritability, aggressive and violent outbursts, and
drug and alcohol abuse. His brain, too, showed CTE affecting widespread parts of his
cerebral cortex and deep brain nuclei. Brains from 3 other college football players
showed similar changes.
Lastly, I have had the opportunity to examine the brain of a high school football player
who died at the age of 18. He had played football and other sports for 4 years and
suffered several concussions. The brain of an 18 year old should be pristine, there
should be no abnormalities anywhere, no abnormalities whatsoever. But in the brain of
this young man, a brain that should be entirely normal, there were spots of undeniable
pathology. They were 4 areas of damage in the frontal lobe that you could see even
looking at the slides with your naked eye (Figure 5). In those areas, there were hundreds
of degenerating nerve cells containing tau neurofibrillary tangles and disordered nerve
12
cell processes. Even in this 18 year old high school student, with only a few years
experience playing football, there were signs of the earliest stages of CTE. Had he lived
longer, this 18 year old would have almost certainly developed the same full blown CTE
that we found in the other college and professional football players.
Figure 5
I have now examined the brains of 7 former NFL players, and 4 college layers, and all 11
have shown profound and widespread changes of CTE. I have also found CTE in a
college level player and the earliest signs of CTE in a high school football player. I
realize that this is just a handful of cases, so – so what? -what can you say from just 11
cases? Well, I can say that for the past 23 years, I have looked at thousands of brains,
from individuals from all walks of life, of all ages, and during the past 20 years, I have
primarily focused on abnormalities of tau protein. But I have only seen this unique
13
pattern of changes, in this severity, in individuals with a history of repetitive head trauma,
including boxers and football players. These changes are dramatically not normal -there
is no way these pathological changes represent a variation in normal that we find under
a bell shaped curve. We have found these changes in every professional football
players’ brain that has come into my laboratory at the BU Center for the Study of
Traumatic Encephalopathy and I have never seen this in 20 plus years of examining
brains. I have had colleagues of mine from other institutions – leading neuropathologists
from Harvard and Mt. Sinai—independently examine these brains, and they have come
up with the same diagnosis as I had, CTE. I know that the argument is often made that
there are hundreds of thousands of former football players, including former professional
football players, with no signs of any cognitive decline or memory loss or personality
change, but what I don’t understand is why are we expecting that this exposure to
repetitive head trauma will have 100% penetrance into the population and cause disease
in every football player? Do we expect 100% of cigarette smokers will develop lung
cancer? Do we expect 100% of children who play with matches or even chain saws will
get hurt? No. Even if the percentage of affected players is 20%, or 10%, there are still
thousands of kids and adults out there, right now, playing football at all levels -who will
eventually come down with this devastating and debilitating disorder. And as a doctor
and as a mother, I think this calls for immediate action. We need to take radical steps to
change the way football is played and we need to make those changes today.
14
B.U. Center for the Study of Traumatic Encephalopathy Grant Support
Title: Development of Pathology Diagnostic Criteria for Chronic Traumatic
Encephalopathy
Co-Principal Investigators: Ann McKee and Robert Stern
Type of Grant: Supplement to P30 Center Grant (N. Kowell, P.I); P30-AG13846
Funding Agency: National Institute on Aging
Years Funded: 2009-2010
Total Direct Costs: $83,287
Title: Neuropathologic Examination of Traumatic Encephalopathy in Athletes with
Histories of Repetitive Concussion
Co-Principal Investigators: Ann McKee and Robert Stern
Type of Grant: Supplement to P30 Center Grant (N. Kowell, P.I); P30-AG13846
Funding Agency: National Institute on Aging
Years Funded: 2008-2009
Total Direct Costs: $100,000
JAMES CRISP / Associated Press
Boyd Martin riding Neville Bardos at the 2010 World Equestrian Games in Lexington, Ky. "He's always been overenthusiastic at everything he does," Martin says of the chestnut horse.
Just after 1 a.m. on May 31, the rolling hills of True Prospect Farm in Chester County lit up as a fast-moving fire raced through a barn housing 11 show horses.
Stable workers pulled four to safety, but Neville Bardos, a big chestnut contender for the 2012 Olympics, was trapped in his stall.
With hay and straw ablaze, firefighters thought it too risky to try to save him. Neville's Australian-born trainer, Boyd Martin, had different ideas. He briefly argued with the fire crew, then broke past and ran into the burning barn.
"I held my breath as deeply as I could - I couldn't see anything, but I remember hearing a gurgling," Martin said. "[Neville] was cooped up in a corner and I reached out and found his shoulder and then I found his neck. I got my hand around his neck collar but couldn't move him. He was panicked."
At that moment, Martin's friend and the barn's owner, Phillip Dutton, emerged through the smoke. With Dutton pushing hard from behind, they managed to drag Neville down the aisle and into the crisp May air.
"If I had left it another 30 seconds," Martin said, "it would have all been all over."
With Neville's lungs and airway heavily damaged by smoke, there was no thought that night of whether the horse Martin had named for an Australian gangster would ever compete again - only whether the vets could keep him alive.
Remarkably, the 13-year-old with two white socks and a big white blaze on his face not only resumed competing but was recently awarded the sport's highest honor: Horse of the Year, chosen by the United States Equestrian Federation. Another horse, Sjoerd, shared the award.
Martin, who rode Neville to seventh place in the world's most important cross-country races, the Burghley Horse Trials in England, just three months after the fire, wasn't surprised.
"What that horse did on and off the competition stage last year, I couldn't see a horse in the world that could beat him," he said.
A USEF spokeswoman agreed.
"If he'd gone to live in Boyd's backyard for the rest of his life, the story would have had a happy ending," said Joanie Morris. "But to jump around one of the toughest competitions in the world, that's remarkable."
Six top show horses died in the Memorial Day weekend blaze, which Chester County fire officials say started accidentally near a hay steamer in the center of the barn. Of the five that were rescued, Neville was among the worst off.
Caitlin Silliman, who works for Martin as an assistant rider, was asleep in an apartment above the barn when she and her two roommates heard the horses whinnying and shaking in panic.
They raced downstairs to open as many stall doors as they could, but the horses were too scared to move. They dragged out four before Martin arrived.
"The whole thing lit up very quickly," recalled Silliman.
Her own horse, Catch a Star, suffered burns over 50 percent of her body.
Neville, she said, was "really lucky" to escape serious burning. Silliman was even luckier; her apartment shared a wall with the hayloft.
The horse's worst injury was to his upper airway and lungs, said Samantha Hart, the veterinarian who saw him for almost two weeks at the University of Pennsylvania's New Bolton Center. He then was treated in a hyperbaric oxygen chamber at Fair Hill Equine Center.
Hart said the horse's injuries could have ended his career, but "he's definitely a fighter. He's an amazing horse."
That's hardly the way anyone would have described Neville when Martin bought him for $800 as a washed-up 3-year-old racehorse destined for the slaughterhouse - his first brush with death.
"I thought he looked like a real athlete," said Martin, who planned to train him as a jumper and sell him.
But the horse turned out to be a handful and a "wind sucker," a bad habit in which horses bite and chew on whatever they can get their mouths on and suck up air, which can cause colic.
"I was stuck with him," said Martin, who named him after another hothead, a notorious Australian gangster.
Silliman is more blunt: "He's wild. A lot of the girls at the barn won't even walk him. He gets spooked and runs and tries to buck you off. He's a very unpredictable horse."
But he's also fast and strong and a hard worker. Neville's sport, eventing, consists of three parts: a cross-country obstacle course, show jumping, and dressage. Slow on the track, Neville rockets around the open fields of a cross-country course.
"I'm sure he was put on this earth to do it," said his trainer, who sold him to a 10-member syndicate in 2010 for $150,000.
Dressage is his soft spot. The series of controlled movements requires elegance, precision, and suppleness, qualities that don't mesh with Neville's exuberance.
"He's always been overenthusiastic at everything he does," Martin said. "He almost tries too hard to please."
After a rough start, Neville started winning events and was short-listed for the 2008 Beijing Olympics. In 2010, he was named to the U.S. team for the World Equestrian Games and ended up being the highest-placed U.S. horse.
Now Martin and his wife, Silvi, a dressage trainer and rider, are waiting to hear about this summer's Olympic Games in London, which will commemorate the centennial of the equestrian event. Martin had been a contender for the Australian team for many years but now will try for a berth with the United States.
"That's the pinnacle of our sport," he said of the Olympics.
And riding to gold atop his miracle horse, he said, "would be huge."
