23 November 2013
1349 hrs
And a good day to you all, Patient Reader . . .
The weeks past had some interesting developments:
1)
There
are just some things in life for which some people, Buddhist or not, can ever
forgive another. I keep saying, and
believing, that none of us is only the worst thing we have ever done, or have
been accused of doing. How sad for those
hypocrites who spout their liberal understandings; their compassion over
suffering and desire; yet get wind of something, true or untrue, never bother
to sort out the facts, never desire for themselves an explanation, and just run
pell-mell through the world exacerbating situations. Joke ‘em if they can’t take a fuck.
2)
I
was honored, in a bittersweet sort of way, by a classmate who tried to “play
matchmaker” (her words) with yours truly and some mystery woman.
“She’s smart and beautiful . . .” (and you know too well,
Patient Reader, that I feel beauty is not important . . . to me, all smart women are beautiful) this
classmate tells me. “I told her all
about you and she was all, ‘Oh my God’.”
“I’m really not in a position to try a new relationship,” I
tell this girl . . . we’ll call her
Shmauren. “I am just too busy with
school to try anything new.” The
bittersweet? Bitter was that it was not for one of Shmauren's contemporaries. That I am no longer considered (nor have I been for quite some time now, I reluctantly admit) desirable by the "Young and Beautiful People." It was to be for
her mom, this set-up.
Sweet? That it was to be for her mom. Contradictory? Nope.
What an honor for a guy who is found so appealing that someone would try
to set them up on a date with his or her mother. I mean, flattering, right? The compliment . . . The trust! And-
3)
The
PAC NW can get brutally cold. It’s only
the end of November and we’ve dropped into the low 20’s, fa chrissakes. How will it be when winter officially gets
here? When January gets here? When Hell finally fucking freezes over?
So really, that’s all the ranting I have to do for now, Kind and Oh-So-Patient Readers. Just pretty ticked at the unforgiving nature of stupid fucking people. Even a cynic, jaded and crusty as I, can understand second chances.
But just for your Sweet Patience, my lovely share-ees, I have another completed paper for you all to peruse at your leisure. As always, your comments, neg or pos, are welcome. Bring them on, as they say.
Without further adieu, I would like to introduce you to “Football Kills.”
Shall we begin? Splendid!
Football
Kills
By
The Ever-Forgivable Cunning Fennec Fox
Or, more accurately perhaps: Chronic Traumatic
Encephalopathy kills.
Chronic
Traumatic Encephalopathy, or CTE, presents clinically with memory disturbances,
changes in behavior and personality, and problems with speech and gait. Dysarthria, dysphagia, and oculomotor changes
are also seen.
Parkinsonian
symptoms present in all known cases.
These include rest(ing) tremors, bradykinesia, and exaggerated startle
reflex. Sub-clinical changes include intrinsic plasticity, wherein
there are changes in the electrical properties within the individual neurons
themselves.
The
areas of the brain that govern memory and speech are primarily in the temporal
lobes. Behavior and personality control
centers are found in the pre-frontal cortex.
Gross motor movement is governed by the motor strips found in the
parietal lobes in both hemispheres of the brain, whereas fine motor skills and
gait are controlled by the cerebellum. The
aforementioned dysarthria, dysphagia, and oculomotor changes are indicators of cranial
nerve root or brainstem damage.
As is
evident by the laundry-list of symptoms, whatever is happening to CTE patients
is affecting the global brain, meaning both hemispheres are involved.
CTE is
caused when a brain, over time, accumulates abnormal tau. Tau is a protein
necessary in the formation and maintenance of neurons. Abnormal tau
is a major component in neurofibrillary tangles. Essentially, excessive tau causes neurons to snarl like old fishing line or Christmas
lights.
The CTE
brain accumulates tau because neurons
damaged via repeated trauma demand this neuronal gorilla-glue in greater amounts than those within the healthy
brain. But the damage is too extensive,
and the protein throws up its hands in exasperation. When the damage still goes unrepaired, more tau shows up, and the cycle continues.
When accumulated thusly, tau damages the very neurons they are
designed to repair and make whole. They
choke off nutrients and actually cause macroscopic regions of brain tissue to
die off. The damage to a CTE-afflicted
brain can be seen with the unaided eye.
Similar
encephalic changes are seen in prize-fighters; a condition known as dementia pugilistica. But those are boxers, are they not?
I am
writing about Professional Football Players.
These guys are not only as tough as boxers, but they wear protective
gear. Gear that boxers would fight over,
were they not so busy fighting over purses and belts. Football players wear all manner of
pads. They tape up their ankles and
wrists to limit lateral, oblique, and anterior/posterior joint slippage; they
wear knee braces and back braces and they have cages called facemasks riveted to their helmets. And let’s not forget they wear helmets in the first place. How does a brain get injured when it’s
wrapped inside a skull that’s wrapped inside a helmet?
Well,
the brain is a fragile organ. First of
all, the formidable skull’s thickness can be measured in millimeters. That’s thousandths
of a meter. Skull bone is tough, but
relatively thin.
Beneath
the cranium are the meninges, the three layers of tissue that surround the
brain and spinal cord in a protective sheath, each layer with its own job to
do. The second and third layers of
meninges are separated by cerebrospinal fluid, a sort of liquid shock absorber
that doubles as a nutrient bath. Blood
vessels responsible for internal respiration are also located here, within the
subarachnoid space. Directly beneath the
third layer, is the surface of the neo-cortex, the outermost layer of the brain
proper.
Helmets
are designed to cushion a lot of the force of the blow. But they can’t stop it all. A professional lineman can sustain a thousand
blows to the head each season he plays, with the blows reaching forces up to 20
g’s. That is the equivalent of driving a
car 35 miles per hour into a wall, one thousand times a year. No helmet made is that good.
Consider also
that when the skull stops from its movement through space, the inertia of the
brain itself is overcome, and it begins its own release of kinetic energy, and
moves in the direction of least resistance (that is, until it meets resistance)
then sloshes back into place. The brain gets injured whether it meets a bullet,
a windshield, or the inside of the cranium.
CTE was
first identified and described in 2002, when Dr. Bennet Omalu, a trained
neuropathologist, autopsied a professional football player by the name of Mike
Weber. Weber played for the Pittsburgh
Steelers from 1974 to 1990. He was fifty
years old when he ended up on Omalu’s slab.
Upon gross
examination of the cadaver, Omalu was surprised that Weber was only fifty years
old, as he appeared to be in his seventies.
Omalu suspected that Weber’s brain would show signs of the advanced
deterioration seen in late-stage Alzheimer’s Disease, but upon macroscopic
examination the brain appeared normal.
He then
fixed slides of brain slices and discovered that there was an unusually high
build-up of tau evident globally,
with most accumulation in the gyri and
sulci of the cerebral cortex. This was the neuropathological “smoking gun.”
Repetitive
closed head trauma has been described in contact sports across the board
(including, but not limited to): boxing, wrestling, lacrosse, skiing, rugby,
and soccer, as well as football.
Though
the chronic neuroencephalopathies associated with repetitive brain injury are
best known in boxing (in the form of dementia
pugilistica), verified CTE has been identified in professional football
players, professional wrestlers, and soccer players, as well as those suffering
from seizure disorders, head bangers*, and domestic abuse victims. People beating their loved-ones into brain damage.
Post-Concussive Syndrome has also been
identified in those participating in hockey, rugby, martial arts, horse riding
and parachuting.
So I am
torn between my love of sports and my passion for neurophysiology. The dichotomy is plain to see when I ride my
motorcycle to the hospital after being called in to determine brain death in a
patient. The neurosurgeon on call
proffered a Donor Card once, and I pulled my own out of my wallet.
I think
of all the hits I put on other players while playing ball, and all the ones
they put on me. I think of the kicks to
the head I sustained in martial arts, and the snowmobiling accident that
damaged my knee and almost broke my nose as my face shattered the windscreen.
I think
that all contact sports will continue to experience head trauma; it has also
been determined that sub-concussive injuries lead to the same encephalic damage
that precipitates CTE. But neither big
hits nor the injuries they cause will ever be eliminated from football.
Just
the hits sustained by kids in Pop Warner Leagues are enough to bring about the
precursors of the disease. How many
subclinical injuries have been sustained by the child before he or she even
enters high school?
If just
ten-percent of mothers refused to let their kids play football, the NFL would
collapse. This is why the NFL has been fighting Dr. Omalu et al with all their might.
Only recently have they reluctantly began to acknowledge even the mere existence of CTE. To the NFL’s credit, they, without any
admission of responsibility, donated $50 million to Boston University, where
the research on CTE began in earnest.
Sports
are integral to Man, to Homo Sapiens
Sapiens. Evidence of sports has been
found in cultures thousands of years gone.
The Sumerians raced horses. The
Assyrians, Hittites and Egyptians had chariot races; we all know about the
Greeks and their Olympics. The Romans,
of course, had the Gladiatorial “games.”
As a
species we compete, perhaps a throwback to the times when physical prowess
attracted a mate. We are a species prone
to violence as default; our hypothalami demand action in stress situations. We started wars for land, and we evolved to
wars of attrition. We will always cheer
the hard hits, yelling “Get him! Knock
him OUT!” and we will never sate this
oddly attractive thirst.
Knowing
what I know about neurophysiology, I would be hard-pressed to permit a child of
my own to play football. “Want to be an
athlete? Be a danseur/ballerina. They’re
the true athletes,” I would tell him or her.
“And they have much fewer head injuries . . .”
* The use of the term, "head bangers" may not be exactly what you think it is. Headbanger is a term used in medicine for those who repeatedly bash their crania against the wall or floor or other sturdy object. This usually presents in those who are mentally ill or neurologically challenged, as if those afflictions aren't cruel enough.
Works Cited
Kirk, Michael, Mike Wiser,
Steve Fainaru, and Mark Fainaru-Wada. "Frontline." League
of Denial. Prod. Michael Kirk, Jim
Gilmore, and Mike Wiser. Dir. Michael Kirk.
PBS. 08 Oct. 2013. Watch PBS Online | PBS Video.
PBS.org. Web. 16 Nov. 2013.
<http://video.pbs.org/>.
McKee, Ann C., MD, Robert C.
Cantu, MD, Christopher J. Nowinski, AB, E. Tessa
Hedley-Whyte, MD, Brandon E. Gavett, PhD, Andrew E.
Budson, MD, Veronica
E. Santini, MD, Hyo-Soon Lee, MD, Caroline A. Kubilus,
and Robert A. Stern,
PhD. "Chronic Traumatic Encephalopathy in Athletes:
Progressive Tauopathy
following
Repetitive Head Injury." Journal of Neuropathology and Experimental
Neurology 68(7) (2009):
709-35. Web.
McKee, Ann C., MD, Brandon E.
Gavett, PhD, Robert A. Stern, PhD, Christopher J.
Nowinski, AB, Robert C. Cantu, MD, Neil W. Kowall, MD,
Daniel P. Pearl, MD, E.
Tessa Hedley-Whyte, MD, Bruce Price, MD, Chris Sullivan,
Peter Morin, MD,
PhD, Hyo-Soon Lee, MD, Caroline A. Kubilus, Daniel H.
Daneshvar, MA, Megan
Wulff, MPH, and Andrew E. Budson, MD. "TDP-43
Proteinopathy and Motor
Neuron Disease in Chronic Traumatic Encephalopathy."
Journal of
Neuropathology & Experimental Neurology: 69.9
(2010): 918-29. Print.
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