Skip to content

Treatment that works!

January 6, 2016

Hi everyone, as some of you know I have been recovering from a TBI (Traumatic Brain Injury) and PTSD as the result of a major accident in 2013.  I was in neuro-rehab for months and continued treatment until benefits ran out when I was released from my job — as I couldn’t do what I used to do anymore.  My endurance, my memory, my emotions, my ability to handle stress all went downhill after my accident.  My family and I came to accept ‘this was the new me’… but deep down I felt there was something that would help me recover.

I tried the pharmaceuticals my neuro-rehab doctor prescribed to help with the lingering symptoms, and various natural treatments, but nothing worked well.  I was constantly exhausted, overwhelmed in public and stressful situations.  I was depressed and knew that I had to find a way to come back… my daughter kept saying she missed her Mommy and my husband said I wasn’t the woman he married.

Thanks to two new friends and colleagues, Dr. Marilyn Faulkenberg and Lisa Gentner, I was introduced to Nerium.  We were having lunch and the conversation turn an unexpected turn to the topic of CTE (Chronic Traumatic Encephalopathy).  I got goosebumps as they told me about Nerium’s EHT supplement and how it impacts the Tau protein that builds up in the brain after trauma, stress, and head injuries.  Lisa gave me a box to try, and I still can’t believe it!  I FINALLY found something that worked for me, and now my husband, my father, and three of my friends have been taking EHT; all of them are having amazing results!  They are describing what I have been experiencing:  we are focused, we are sleeping better, the ‘fog’ is lifting, our memories are better – and for me personally, my overall ‘fight or flight’ has diminished dramatically!

EHT is not just for CTE/Traumatic Brain Injury, it’s for Alzheimers, ADHD, and anyone who is looking to enhance brain function and health.

I shared the product ingredients information with one of my neuro therapists. He said everything in it is what he and his wife take (Selenium, B12, B6, D, Magnesium, among other natural supplements), but he didn’t realize it came packaged this way.  For those of you who want to understand what I’m taking look up Nootropics – there are various ones. This is the only one I am ‘endorsing’ given the results we’ve had.

I chose to be a Brand Partner for Nerium, because I believe in it so much – and with that said, I am going to give away one box of EHT a month.  If you want to be entered in a random draw, please like and share this post via Facebook or email me and let me know you shared it through email with someone you think could benefit from the EHT supplement.

I am adding a link to provide more information (technical) and a link to my Nerium web site.  If you want to purchase a 30 day supply, it is $55 through my site ($75 retail) and there is a 30 day money-back guarantee.  Please give it some time to work, as some people have needed up to a month to see changes – some just hours.  I had a slight headache the first day, but I realized my brain was waking up.  It was actually a cool experience when I recognized what was happening.  My husband found the EHT starting working over the first night.  He woke up the next morning and said the heaviness and chatter were gone.  We both are energized, focused, and so much clearer.  My memory is back.  That too was an interesting experience as it felt like my memory was worse for a few weeks, but I realized the neural pathways were being created as areas of my brain re-awakened.  I’m remembering phone numbers again (couldn’t remember my husband’s work phone number!!!) and I’m not getting lost driving around like I used to.  I have some lingering physical and visual disabilities caused by my accident; otherwise, I would say I am better than I was before the accident!

If you know anyone who is battling CTE or brain injury related memory loss, confusion, depression, ADHD, please consider EHT.  I can’t promise it will work, but it does provide some hope for our family, especially given the trauma we have had.  For those of you who don’t know about my brother, Sean – he killed himself in 2012 after years of battling what we now understand to be CTE.  This disease SUCKS!  Alzheimers is stealing our elders and that SUCKS!  So many people I have met are desperate for help and I haven’t been able to do anything through HeadsUp CTE other than provide awareness.  I finally found something that I believe in with all my heart.  I will continue to post information, videos, and endorsements from people like NFL Super Bowl athletes Steve Weatherford and Sidney Rice who take and promote Nerium’s EHT (below).  Please let me know if you have any questions! (email)


My Nerium page on EHT.

Ingredients list:  Vitamin D (as cholecalciferol) • Vitamin B6 (as pyridoxine HCl) • Folate (as folic acid) • Vitamin B12 (as cyanocobalamin) • Magnesium (from 100 mg magnesium citrate) • Selenium (as selenomethionine) • Huperzine-A (from Huperzia serrata whole plant extract) • Alpha lipoic acid • EHT® (proprietary coffee extract) • Dicalcium phosphate • Microcrystalline cellulose • Coating (polyvinyl alcohol, titanium dioxide [color], macrogol, vanillin, talc) • Croscarmellose sodium • Stearic acid • Magnesium stearate • Silica

Recovering from my own concussion…

December 31, 2013

On November 10th 2013, I fell down a flight of stairs while moving into our new house.  In addition to shattering my wrist and causing some major damage to my body, I hit my head (I don’t know how many times), as I rolled down the stairs.  I have been told multiple times that I am lucky to be alive.

Of all people we, including myself, should know better, but we didn’t deal with my concussion early on.  I think we were in such shock from the physical injuries, the immediate surgery that resulted from my injuries, the pain medications, adjusting to a new home in a new state, and just the overall chaos, we didn’t really think about how my head was doing.  In the ER, I also insisted that my head was fine, and because of the obvious injuries that needed to be taken care of, no one pressed me about a possible concussion.  I slept most of the first 10 days and we assumed that was because I was on major painkillers.  I would wake up with terrible headaches, I couldn’t read, couldn’t remember words or trips or names, and all in all I couldn’t think clearly – but again we attributed it to everything else going on.

Three weeks after I fell, we realized I was suffering from Post Concussion Syndrome. I went to see a doctor to get confirmation, and although she saw signs of a concussion she basically said there was nothing she could do. She told me to come back in two weeks with somebody who could vouch for my sanity as for all she knew, I was making the entire story up, and just wanted more pain killers.  She did say to rest for three weeks, I when I told her I had, she said I should be ok with a little more rest.  After that wonderful experience, we took matters into our own hands.  We called our local Brain Injury Association and got referred to a Dr. who specialized in brain injuries from concussions.  I also decided to start acupuncture immediately, weaned myself off the pain killers, and began taking an intense regimen of high quality omega 3’s, homeopathic Arnica Montana, and other multi-vitamins.

I was already going to physical therapy three times a week for my wrist, arm, shoulder, and back, and mentioned to my PT what happened regarding the concussion.  It turns out that in the state of Kentucky you don’t need a prescription for physical therapy.  So I signed up for the concussion management therapy.  I must admit it has helped quite a bit, even though I still have vision and vestibular issues, my mood has not been the best, but my memory has been returning slowly.  Its one day at a time right now.

This is at least my 10th concussion in 44 years.  Not a statistic I’m proud of, but I too was a competitive athlete, was in major car accidents as early as my elementary school days, and seemed to be magnetically attracted to trees and buildings when skiing.

The one thing I would encourage everyone to remember is that after a head injury, symptoms may not show up for days.  For me it was about 10 days.  And don’t give up the fight for what you know is right.  Do what you need to do, even if the medical industry does not agree.  It wasn’t easy getting help for a concussion or post concussion syndrome.  The doctors knew what to do with broken bones and shattered wrist, they had no idea how to help a head injury even in the ER.  Find the right people, find an advocate, call your local Brain Injury Association (even if you only suspect that a concussion is possible) and don’t give up!

Discussion forums for those impacted by CTE

August 27, 2013

The Sports Legacy Institute has set up two web-based communities for those impacted by head trauma.  The purpose of the forums is to provide two separate and exclusive places for safe and secure communications among:

1.         People with a history of exposure to head trauma through contact sports or military service who have been diagnosed with, or suspected to suffer from CTE.

2.         Family members and caregivers of those who show symptoms of CTE. 

Thank you SLI for this wonderful resource!


Today is 5 ~ 4 Day! Help us with our mission: “Concussions last more than a lifetime…”

May 4, 2013

Hello all,

It has been just over a year since Sean’s death, and it still amazes me how many people are posting on his Facebook page, how many people are contacting us after just learning about his death, how many people are sharing stories of how their lives have changed because of Sean.

Almost as powerful is the number of people who have been in touch with us since we formed our non-profit Heads Up! CTE in November of 2012.  We have had over 5000 hits to this web site, with people from around the world asking for resources and information for their sons, daughters, fathers, mothers, spouses, friends, and themselves…

Sean’s legacy lives on, he continues to help so many people with his story, his pain, his achievements — despite the disease that slowly destroyed his mind.

In the past couple of months we have had some major milestones, and today, May 4 (5~4), I want to share those with you — in honor of my brother, Sean O’Malley who’s favorite number and sports jersey number was 54 for much of his football career:

1) Numerous high schools, colleges, and little league football teams have been using materials and information we have provided to educate their coaches, physicians, players and parents about the risks associated with repeated head injuries.

2) State legislators and other public officials have been referring to our web site and resources.

3) We have been featured in various web and print publications with a special focus on Sean’s story.

4) Bishop Ireton High School, where Sean attended in Virginia, will award the first Sean O’Malley Memorial Scholarship to a very deserving student-athlete on May 23rd, 2013.

And, something that we need your help with:

On May 22, 2012 my parents, Jeff and I will be heading to Washington, DC to attend the Tom McHale Memorial Event for the Sports Legacy Institute.  At this event we will be meeting with NFL players, members of the NFL organization, the who’s who in the field of research, education, and treatment for Chronic Traumatic Encephalopathy (CTE), legislators, and others who are actively searching for resources and cures for CTE.  HeadsUp! CTE is committing to being sponsors which will allow us to share Sean’s story with so many in such a powerful way, and we are looking to raise at least $1000 for this event.  We welcome your donations to help sponsor, and in continued support of our efforts.

In honor of 5 ~ 4 Day and to thank you for your donation, we are offering an unreleased and inspiring audio track recorded by Sean during the production of the Volume 5 Cardio Coach(TM) workout.  We will provide a link to this gift of Sean with each donation.

Heads Up! CTE is a non-profit organization, so your donation is tax deductible.  Please save the Pay Pal receipt for your files.

Here is the link to make a donation:

After making your donation — please click on the button that allows you to continue to our website — and follow the instructions to download the audio file.

Thank you for your continued support as we spread the word about the link between head injuries, contact sports, and CTE.

With love and appreciation,

Colleen, Jeff, Chuck and Nancy

5 ~ 4 DAY

Four Stages of CTE Found in Latest Boston University Study

January 25, 2013


By looking at the extent of the diseased areas, the researchers determined which brains were stage I, II, III, or IV CTE. And by conducting interviews with the families of the deceased, they were able to figure out how the progression of behavioral and emotional symptoms corresponded to each stage of the disease.

Here’s how they categorized them:

Stage I: This stage is marked by headache and loss of attention. It may also include short-term memory problems, depression, and aggressive tendencies. A couple of the individuals had had problems with executive function and explosivity.

Stage II: In this stage, individuals were more likely to have experienced headache, attention and concentration problems, mood swings, short-term memory loss, and impulsivity. Less commonly they may have also experienced suicidal thoughts and language problems.

Stage III: This stage is marked by the symptoms of the previous stages, with the possible addiction of visuospatial difficulties, more extensive cognitive and memory problems, and apathy. The authors say that at this stage, 75% of the individuals “were considered cognitively impaired.”

Stage IV: This stage is commonly associated with more significant cognition problems and memory loss. “Most subjects also showed profound loss of attention and concentration, executive dysfunction, language difficulties, explosivity, aggressive tendencies, paranoia, depression, gait and visuospatial difficulties,” the authors say. Over 30% were suicidal at some point, and a few experienced problems with physical movement known as parkinsonism.

Interestingly, 37% of the people with CTE also had another neurodegenerative disease, including Alzheimer’s, FTD, Lewy body disease, or Parkinson’s, which could suggest that once CTE develops, it can trigger other pathological pathways.

Concussions Don’t Cause CTE…

January 25, 2013

Results from various studies, including one using high school football players are showing repetitive hits, not concussions, are causing short and long term brain damage:


On Feb. 3, Purdue University released an analysis of concussions among high-school football players by the Purdue Neurotrauma Group. Based on brain scans, the researchers determined that concussions “are likely caused by many hits over time and not from a single blow to the head, as commonly believed.”

In the study, researchers studied football players for two seasons at Jefferson High School in Lafayette, Ind. During the first season, according to the university, 21 players completed the field test, while 24 completed it in the second season, including 16 repeating players.

Players used helmet sensors, from which researchers compared impact data with brain-imaging scans and cognitive tests performed before, during and after each season, the university stated.

MRI scans of the players found that, as players got hit more and more, brain activity changed, and the players began to adapt their mental processes to deal with those changes. Essentially, the study found, the more impacts, the less functional capacity they had, and players then had to use a different strategy to perform a task at the same level as before.

So while performance might not have noticeably changed, brain activity did, the researchers found. And, the more hits a player took, and the more brain activity change there was, the more likely a concussion was to occur over time, according to the scan results.

“The most important implication of the new findings is the suggestion that a concussion is not just the result of a single blow, but it’s really the totality of blows that took place over the season,” said one of the researchers, Eric Nauman, an associate professor of mechanical engineering and an expert in central nervous system and musculoskeletal trauma. “The one hit that brought on the concussion is arguably the straw that broke the camel’s back.”

Read more here:



Once You Have a Head Injury – updated

January 23, 2013

…in Any Sport

REMOVE athlete from play

REFER to medical provider

REST no sports, no texting/TV  — LET THE BRAIN HEAL

RETURN only with doctor’s OK

Source:  Children’s Hospital Boston, Sports Concussion Clinic

The following is excerpted from:

Danger Signs — Adults

In rare cases, along with a concussion, a dangerous blood clot may form on the brain and crowd the brain against the skull. Contact your doctor or emergency department right away if, after a blow or jolt to the head, you have any of these danger signs:

  • Headaches that get worse
  • Weakness, numbness, or decreased coordination
  • Repeated vomiting

The people checking on you should take you to an emergency department right away if you:

  • Cannot be awakened
  • Have one pupil — the black part in the middle of the eye — larger than the other
  • Have convulsions or seizures
  • Have slurred speech
  • Are getting more and more confused, restless, or agitated

Danger Signs — Children

Take your child to the emergency department right away if the child has received a blow or jolt to the head and:

  • Has any of the danger signs for adults
  • Won’t stop crying
  • Can’t be consoled
  • Won’t nurse or eat Although you should contact your child’s doctor if your child vomits more than once or twice, vomiting is more common in younger children and is less likely to be an urgent sign of danger than it is in an adult.

Symptoms of Brain Injury

Persons of All Ages

“I just don’t feel like myself.”

The type of brain injury called a concussion has many symptoms. These symptoms are usually temporary, but may last for days, weeks, or even longer. Generally, if you feel that “something is not quite right,” or if you’re “feeling foggy,” you should talk with your doctor.

Here are some of the symptoms of a concussion:

  • Low-grade headaches that won’t go away
  • Having more trouble than usual:
    • Remembering things
    • Paying attention or concentrating
    • Organizing daily tasks
    • Making decisions and solving problems
  • Slowness in thinking, acting, speaking, or reading
  • Getting lost or easily confused
  • Neck pain
  • Feeling tired all the time, lack of energy
  • Change in sleeping pattern:
    • Sleeping for much longer periods of time than before
    • Trouble sleeping or insomnia
  • Loss of balance, feeling light-headed or dizzy
  • Increased sensitivity to:
    • Sounds
    • Lights
    • Distractions
  • Blurred vision or eyes that tire easily
  • Loss of sense of taste or smell
  • Ringing in the ears
  • Change in sexual drive
  • Mood changes:
    • Feeling sad, anxious, or listless
    • Becoming easily irritated or angry for little or no reason
    • Lack of motivation

Young Children

Although children can have the same symptoms of brain injury as adults, it is harder for young children to let others know how they are feeling. Call your child’s doctor if your child seems to be getting worse or if you notice any of the following:

  • Listlessness, tiring easily
  • Irritability, crankiness
  • Change in eating or sleeping patterns
  • Change in the way they play
  • Change in the way they perform or act at school
  • Lack of interest in favorite toys
  • Loss of new skills, such as toilet training
  • Loss of balance, unsteady walking

Older Adults

Older adults with a brain injury may have a higher risk of serious complications such as a blood clot on the brain. Headaches that get worse or an increase in confusion are signs of this complication. If these signs occur, see a doctor right away.

Trust your instincts.  If you see any changes in behavior, mood, or thought — please seek medical assistance.

Read more here:


Avoiding MSG and Aspertame (NutraSweet/Equal) following head injuries

August 23, 2012

Technical but informative — worth the read – from the blog of Dr. Jack Kruse, a neurosurgeon/nutritionist.


In the first two blogs (1) (2) in this series we looked at the fundamental neurobiology of how excitatory neurotransmitters and exogenous food additives can cause human disease. We discussed that the mechanism of disease progression is affected by age, species, and the energy status of the neuron at the time of exposure or injury. Today we are going to explore how acute neurologic aspects of cranial trauma relates to progression to long term neurodegenerative disease. We also must remember that these athletes, soldiers, and high school students are simultaneously ingesting huge amounts of MSG and aspartate in a standard American diet. I would hope that every person reading this would avoid exogenous sources of excitotoxins going forward. This is especially true if you have sustained a traumatic brain injury or a concussion in your lifetime. Realize that even one concussion can cause this affect to steam roll if you either continue to add insult to the injury exogenously (MSG or Aspartame) or endogenously (injury or disease). Traumatic brain injury accounts for more than 1 million emergency room visits each year. According to the Centers for Disease Control and Prevention, an estimated 3.8 million sports and recreation-related concussions occur in the U.S. each year. So most of these injuries never come for any treatment at all. Moreover, MSG and aspartame sensitize injured human nerves to the effects of acute concussion when they occur. The more processed food you eat as an athlete, the more likely you will suffer long term damage from your concussion.

Concussions, MSG and Alzheimer’s are basically the same disease at different points on the continuum of neuropathology. This explains why so many former NFL players suffer from addiction, depression, neurodegeneration, cognitive decline, obesity, and decreased longevity. Their should be recommendations made to offset the damage based upon what we know. In my opinion not enough is being done. I treat post concussive syndrome much more aggressively and quite differently than most of the published guidelines because I feel I understand the neurobiology and the connections to other diseases we mentioned in this blog. I don’t believe many others do. And those who do wont act because their is an expensive price tag tied to what should be done. The more they muddy the water the longer the status quo can exist.

Full Post

Understanding CTE – causes and the ‘science’ behind it…

August 16, 2012

Found a few publications this morning as I was trying to understand the depositing of the Tau protein better — in a less clinical way.  There are two articles listed here with excerpts.  Once I got past the ‘technical’ and just tried to understand the ‘big picture’ I found myself understanding CTE a bit better.


Repeated blows to the head — from football tackles, blasts from a circus cannon or some other trauma — put the brain at risk for CTE. Although typically associated with concussions or serious head injuries, brains of football players with CTE but without any concussive history demonstrate that repeated, less severe “subconcussive” injuries provide sufficient trigger for this disease. While individual trauma may produce short-term symptoms, the effects of CTE manifest years after the injuries as the disease progresses and the brain breaks down. Yet many athletes with recurrent head injuries evade CTE; it appears repeated head trauma are necessary, but not sufficient, to trigger CTE. Researchers believe that the nature of the head trauma — and the severity, frequency, and age of the recipient — may play a role in whether or not CTE develops. But, for now, why the disease overtakes some and spares others remains a mystery.

The answer hides somewhere amidst tangled neurons and wasted brain tissue. During autopsy, scientists diagnose CTE through the pattern of brain decay and the buildup of tau protein. Normally, the tau protein stabilizes the brain cell skeleton. In both CTE and Alzheimer’s, two distinct diseases, enzymes cause the protein to release from the skeleton and cluster in cells to form neurofibrillary tangles (NFTs). Researchers remain uncertain about the tangles’ exact effect on the brain, says Dr. Brandon Gavett, a neuropsychologist at the University of Colorado-Colorado Springs. Unlike Alzheimer’s, which is characterized by the even spread of NFTs, in CTE, NFTs cluster around blood vessels and dead tissue. According to Gavett, some researchers hypothesize that damage to blood vessels during head trauma may cause the brain to wither and form NFTs but thus far no mechanism of disease has been proven.

Brain damage associated with CTE triggers crippling psychological effects. Because the disease can only be diagnosed by autopsy, the changes in behavior and mood must be pieced together by interviews with family members after the afflicted person’s death. Family members report that their loved ones exhibited problems with learning, remembering new information, and organization. Judgement and impulse control also frequently gave way to aggressive behavior and problems with addiction. Additionally, those affected by CTE frequently became depressed, agitated, and — in what ultimately takes the lives of many with CTE — suicidal. On top of these emotional changes, difficulty with balance, gait, and speech similar to Parkinson’s disease often accompany CTE.

Despite the wealth of symptoms identified, these psychological factors need to be integrated with genetic susceptibility, chemical analysis of blood and cerebrospinal fluid, and brain imaging in order to accurately diagnose CTE in living patients. Possible chemical markers and genetic predispositions for CTE have been identified from research on Alzheimer’s disease, and pilot studies show promise for diagnostic MRI and MRS scans as brain imaging technology improves. Late last year, Boston University CSTE began a study of NFL players and non-contact athletes to begin integrating these parts and develop methods to diagnose CTE before death. Some knowledge needed for such a diagnosis still evades researchers, but scientific advancement creeps closer to this goal every day.

Full article


Here is another article that somehow made sense to me. If anyone has the ability to talk through this and help me better understand what this all means, please let me know 😉  If you can get past the ‘technical’ and medical terminology there are some fascinating thoughts and findings that don’t make the mainstream news (probably because it is not an easy read).


CTE is a potential late effect of repeated head injuries

CTE is not thought to be a long-term sequela following a specific head trauma. Rather, its clinical symptoms emerge later in life, usually after an athlete retires from his or her sport. Like most other neurodegenerative diseases that cause dementia, CTE has an insidious onset and gradual course. Based on a recent review of neuropathologically-confirmed CTE in athletes [11,] the mean age of onset is 42.8 years (SD = 12.7; range = 25 – 76 years). On average, onset occurs approximately 8 years after retirement (SD = 10.7), although approximately one-third of athletes were reportedly symptomatic at the time of retirement. In athletes, the course appears to be considerably protracted (mean duration = 17.5 years, SD = 12.1), especially in boxers. The average duration of the disease in boxers is 20 years (SD = 11.7) and 6 years in American football players (SD = 2.9) [11.] If the affected individual does not die of other causes, full-blown clinical dementia may occur late in the course of the disease.

Gross Pathology

Neuropathological studies of athletes with a history of repeated mild head injuries have produced a number of consistent findings that, together, make CTE a distinctive disorder. Upon gross examination, there is often anterior cavum septum pellucidum and, usually, posterior fenestrations. These changes may be caused by the force of the head impact being transmitted through the ventricular system, thereby affecting the integrity of the intervening tissue. Enlargement of the lateral and third ventricles is also a common feature seen in CTE; the third ventricle may be disproportionately widened. Additional gross features include atrophy of the frontal and temporal cortices, atrophy of the medial temporal lobe, thinning of the hypothalamic floor, shrinkage of the mammillary bodies, pallor of the substantia nigra, and hippocampal sclerosis. Atrophy of the cerebrum, diencephalon, basal ganglia, brainstem, and cerebellum, may result in an overall reduction in brain mass [11].

Microscopic Neuropathology


Microscopically, CTE is characterized by an abundance of neurofibrillary inclusions, in the form of neurofibrillary tangles (NFTs), neuropil threads (NTs), and glial tangles (GTs). The main protein composing NFTs is the microtubule-associated protein tau, and NFTs are aggregates of filamentous tau polymers. While CTE shares many microscopic similarities with Alzheimer’s disease (AD) and other tauopathies, it has several distinguishing features. First, the distribution of tau pathology is unique; it is most commonly found in the more superficial cortical laminae (II and III), whereas tau NFTs in AD are preferentially distributed in large projection neurons in layers III and V. Further, the regional tau pathology is extremely irregular, largely confined to uneven foci in the frontal, temporal, and insular cortices, unlike the more uniform cortical NFT distribution seen in AD. Tau NFTs, NTs and GTs are found throughout the medial temporal lobe, often in densities greater than those found in severe AD, and are also prominent in the diencephalon, basal ganglia, and brainstem. NTs and GTs are also found in the subcortical white matter. Finally, NFTs in CTE are most dense at the depths of cortical sulci, and are typically perivascular, which might indicate that disruptions of the cerebral microvasculature and the blood brain barrier that occur at the time of the traumatic injury play a critical role in the formation of NFTs [11.]

Although the precise pathological mechanisms that tie repeated mild head injuries to NFT formation are not known, they may involve a series of diffuse axonal injuries (DAI) set in motion by the initial trauma and aggravated by subsequent mild traumatic injuries. During a traumatic brain injury, the brain and spinal cord undergo shear deformation producing a transient elongation or stretch of axons. Traumatic axonal injury results in alterations in axonal membrane permeability, ionic shifts including massive influx of calcium, and release of caspases and calpains that might trigger tau phosphorylation, misfolding, truncation, and aggregation, as well as breakdown of the cytoskeleton with dissolution of microtubules and neurofilaments [15, 18, 19].

There is also increasing evidence that tau phosphorylation, truncation, aggregation, and polymerization into filaments represents a toxic gain of function and continued accumulation of tau leads to neurodegeneration. This is supported by tau’s involvement in some genetic forms of frontotemporal degeneration [20] and by work that shows that plasmids containing human tau cDNA constructs microinjected into lamprey neurons in situ produce tau filaments that accumulate and lead to neuronal degeneration [21, 22.] However, it is also possible that the intracellular NFTs, in and of themselves, are byproducts, rather than the cause, of cellular injury, and that NFT formation indicates neurons that survived the initial injury and sequestered the abnormally phosphorylated, truncated and folded tau [23.] How a neurodegeneration that starts multifocally around small blood vessels or in the depths of cortical sulci ultimately spreads to involve large regions of brain as a systemic degeneration such as CTE may be explained by a possible tau toxic factor or trans-cellular propagation by the misfolded tau protein [24].


Beta-amyloid (Aβ) deposits are found in 40–45% of individuals with CTE; this is in contrast to the extensive Aβ deposits that characterize nearly all cases of AD. While neuritic plaques are typically abundant in AD and are essential to the diagnosis, Aβ plaques in CTE, when they occur, are less dense and predominantly diffuse [11.] Despite the relatively minor role Aβ plaques appear to play in the neuropathological manifestation of CTE, the role of Aβ in the pathogenesis of CTE has yet to be elucidated. It is known that acute head injuries cause an up-regulation of amyloid precursor protein (APP) production, and that Aβ plaques may be found in up to 30% of patients who die within hours following TBI [25, 26, 27.] DAI, often a consequence of mild TBI, is thought to influence changes in Aβ following head injury. Interruption of axonal transport causes an accumulation of multiple proteins in the axon, including APP, in varicosities along the length of the axon or at disconnected axon terminals, termed axonal bulbs [28.] Although the axonal pathology in TBI is diffuse in that it affects widespread regions of the brain, typically the axonal swellings are found in multifocal regions of the subcortical and deep white matter, including the brainstem. Due to the rapid and abundant accumulation of APP in damaged axons after TBI, APP immunostaining is used for the pathological assessment of DAI in humans. Accordingly, this large reservoir of APP in injured axons might be aberrantly cleaved to rapidly form Aβ after TBI [25, 29, 30.] However, it remains unclear whether the large quantities of APP and Aβ found in damaged axons after TBI play any mechanistic role in either neurodegeneration or neuroprotection [28, 31, 32.] Moreover, it is unknown how long the increased APP and Aβ lasts or what mechanisms may result in variable clearance.


Recently, in addition to severe tau neurofibrillary pathology, we found a widespread TDP-43 proteinopathy in over 80% of our cases of CTE [13.] Moreover, in 3 athletes with CTE who developed a progressive motor neuron disease several years prior to death, there were extensive TDP-43 immunoreactive inclusions in the anterior horns of the spinal cord, in addition to tau immunoreactive GT, neurites, and, occasionally, extensive NFTs. These findings suggest that a distinctive, widespread TDP-43 proteinopathy is also associated with CTE and that, in some individuals, the TDP-43 proteinopathy extends to involve the spinal cord and is clinically manifest as motor neuron disease with a presentation that may appear similar to amyotrophic lateral sclerosis [13.] The shared presence of two aggregated phosphorylated proteins associated with neurodegeneration in the great majority of cases of CTE suggests that a common stimulus, such as repetitive axonal injury, provokes the pathological accumulation of both proteins [33.] Recent studies in vitro and in vivo suggest that over-expression of wild-type human TDP-43 and its dislocation from the neuronal nucleus to the cytoplasm are associated with neurodegeneration and cell death [34, 35, 36.] By virtue of its capacity to bind to neurofilament mRNA and stabilize the mRNA transcript, TDP-43 plays a critical role in mediating the response of the neuronal cytoskeleton to axonal injury. TDP-43 is intrinsically prone to aggregation, and its expression is upregulated following experimental axotomy in spinal motor neurons of the mouse [37.] Traumatic axonal injury may also accelerate TDP-43 accumulation, aggregation, and dislocation to the cytoplasm, thereby enhancing its neurotoxicity.

Immunoexcitotoxicity as a possible central mechanism for CTE. He describes a cascade of events that begin with an initial head trauma, which “primes” the microglia for subsequent injuries. When the homeostasis of the brain is disturbed, some of the microglia undergo changes to set them in a partially activated state. When these microglia become fully activated by continued head trauma, they release toxic levels of cytokines, chemokines, immune mediators, and excitotoxins like glutamate, aspartate, and quinolinic acid. These excitotoxins inhibit phosphatases, which results in hyperphosphorylated tau and eventually neurotubule dysfunction and neurofibrillary tangle deposition in particular areas of the brain [10]. There is also an apparent synergy between the proinflammatory cytokines and glutamate receptors that worsen neurodegeneration in injured brain tissue. This combination also increases the reactive oxygen and nitrogen intermediates that interfere with glutamate clearance keeping the injury response high. Priming can also occur from insults to the brain like systemic infections, environmental toxins, and latent viral infections in the brain (cytomegalovirus and herpes simplex virus) [10].The microglia, however, have a dual function allowing them to switch between being neurodestructive and neuroreparative. During acute injury the microglia are responsible for containing the damage with inflammation, cleaning up debris, and repairing the surrounding damaged tissue [10]. However, if the individual experiences a second brain trauma or multiple continuous traumas, the microglia may never have the chance to switch from proinflammatory to reparative mode [10]. Such repetitive trauma may place the brain in a state of continuous hyperreactivity leading to progressive and prolonged neuronal injury. This would support the evidence that repeated mTBI results in a higher incidence of prolonged neurological damage than single-event injury [10].

Full publication


Treatments Helping Football Player with Mood and Memory

August 4, 2012

This sounds incredibly hopeful!


George Visger was a defensive lineman in the NFL. He said his dream was to play for five years and then retire and build a homestead in Alaska. Things didn’t turn out the way he expected. Today Visger is 51. He is a wildlife biologist in Northern California and has spent the better part of the last 28 years suffering from brain damage, the result of numerous concussions.

Visger played for the University of Colorado in the 1977 Orange Bowl, and many hard hits later, he finished his NFL career with the San Francisco 49ers, playing with the 1981 team that won the franchise’s first Super Bowl.

In one of his earlier emails to me, Visger wrote, “The human body was not meant to play football. My Orange Bowl and Super Bowl rings are not worth what my family goes through dealing with my short term memory issues, anger management issues and lack of judgment.” We talked on the phone last week.

You started hyperbaric oxygen therapy last week. Have you noticed a difference?

Within three treatments I was feeling really different. I’m a lot less tense, and my memory is better. Just remembering your call today—that wouldn’t have happened before. A few months ago I also, started taking some Dr. Barry Sears food supplements—industrial grade Omega 3 and concentrated fruit and vegetable juices, and I think that is helping too.

Full article here.


HeadsUp! CTE in the Charlotte Observer with Kelly Buckley

July 19, 2012

Grieving with gratitude

Charlotte mom shows how giving thanks each day got her through her son’s death

By Alicia W. Roberts, Correspondent, Posted: Friday, Jun. 29, 2012

Kelly Buckley speaks in ripples. Her thoughts cascade off of one another as she scrutinizes her current state of mind and considers the life that brought her to this point.  She’ll claim she is overanalyzing, that her message is much simpler than she’s putting it. Her voice ebbs and flows with each thought – quick and low as she ruminates, stronger and slower as she focuses.

This is her son’s death she’s talking about, so the analysis is understandable.

Stephen, 23, drowned three years ago on the Fourth of July, during an outing with friends at Lake Jordan, near Raleigh. Buckley remembers the unbearable sadness she felt that day. She remembers sitting on the lakeshore, waiting for divers to find Stephen’s body. And she remembers being overwhelmed by the need to write about it all, on the back of a utility bill, in the parking lot of the funeral home after Stephen’s service.

That’s when Buckley began to base her existence on ripples, the ripples Stephen’s life and death could make in the world.

The latest ripple is a new book, “Just One Little Thing,” in which Buckley describes how giving thanks for one thing each day has helped her work through her sadness over Stephen’s death.  “Just One Little Thing” grew out of a Facebook community of the same name Buckley established on July 4, 2011. She posts pep talks and positive nuggets each day for her more than 10,000 JOLT followers. (One post, on a recent Melody Monday: What five songs would be on the soundtrack of your life?)

She pictures Stephen in heaven, urging her on. “His friends said he had a way of figuring out what people needed, and did it,” she said. “I think I’m just continuing what he would do if he were here. … As his mom, that’s what I’m supposed to do.”

Buckley is grateful for the connections she has made with her JOLT-ers, as she calls them.  She has hundreds of emails from readers reaching out; she’ll reply to them all. She has no publicist, no marketer. She’s just a mom, she said, who sits in front of her computer and writes. “The true magic in this is the connections,” she said. “It only happened because I decided to not grieve alone.”

The ripples keep her going, like the one that connected her to Colleen O’Malley-Weber of Charlotte.

O’Malley-Weber’s brother, Sean O’Malley, died earlier this year. He battled with the depression that comes with chronic traumatic encephalopathy, a deterioration of the brain that affects athletes subjected to frequent blows to the head. He took his own life.

O’Malley-Weber calls Kelly Buckley her “virtual sister.” She saw an article about “Just One Little Thing” after her brother’s death, and bought two books – one for her and one for her mother. She said the books – and Kelly’s support – showed her the way to starting, to spread the word about athletes, head injuries and the repercussions.

“When I read Kelly’s book, I learned about the ripple effect,” O’Malley-Weber said. “That kind of cinched it for me. I knew what I had to do.”

Read more here.

Did Football Kill Austin Trenum?

July 18, 2012

This is one of the most powerful articles I’ve read about CTE and high school sports — I’ve pulled some excerpts, however I encourage you to read the article in it’s entirety. If you are prompted to subscribe just click any area outside of the pop up to read the article.


Twelve years ago, Dallas Cowboys quarterback Troy Aikman retired after suffering the tenth concussion of his Hall of Fame career, the result of a vicious hit from Washington Redskins linebacker LaVar Arrington. Aikman since has become a successful broadcaster, a man who owes much to football. After the Super Bowl in February, however, he said that the sport was “at a real crossroads. . . . If I had a ten-year-old boy, I don’t know that I’d be real inclined to encourage him to go play football in light of what we’re learning from head injuries.”

Two football helmets rest on a table. One is black, matte and battered, with an orange mouthpiece wedged in the facemask. The other is reddish and gleaming, decorated with a skull and crossbones and a breast-cancer-awareness sticker. Two gashes run down the front.

The first helmet belonged to Austin. The second belongs to Walker.

Michelle pushes them together. “This,” she says, “is how it happens.”

It’s a Saturday, exactly one year after the weekend of Austin’s death.

Cody finished the previous Brentsville High football season, then quit. He didn’t say why. Walker continued to play for a youth squad, fullback and linebacker, same as Austin. Gil and Michelle didn’t want to overreact, give in to emotion, cocoon their son in bubble wrap. Besides, Austin always took such pride in Walker. The boy loved to hit, so much so that he bragged about it: Mommy, that kid is a baby. He cried, and I didn’t even hit him that hard.

Walker wore a special chin strap, rigged with accelerometers that measured the force of every blow he absorbed. If built-in software deemed any hit powerful enough to cause a head injury, three green LED lights on the chin strap would flash red. While Walker was making a routine block, his head whipped sideways. Red lights. His coach pulled him off the field. Two sideline nurses checked him out. Dizzy and frightened, he cried.

“My head,” he said. “My head.”

The Trenums followed Gioia’s instructions. They made Walker rest. They took him to a Sunday-night bonfire—a memorial for Austin—but didn’t let him run around with his friends. On Monday morning, a neurologist diagnosed Walker with a concussion. Sensitive to light and sound, he was held out of football practice and gym class for a week. One week after that, he was back on the field, Michelle looking on.

“You’re so calm,” one of the other mothers said.

Michelle wasn’t. Watching football on TV was bad enough. This was worse. Also, the chin strap. It was supposed to make things easier, safer. But the lights kept turning red, once when Walker hadn’t even been hit. Michelle made him sit out the entire game. Walker fumed, said he wouldn’t wear the device again. Michelle sent the faulty chin strap back to the manufacturer, got a replacement, then sent that one back, too. More red lights. Was the problem a bad battery? Water leaking into the electronics? Was the problem football?

Michelle wasn’t watching her son. She was watching the lights, waiting for green to go red. She worried about punch-drunk football players, the blows adding up over time—wondered if Walker’s concussion was God’s version of a yellow flag. It was all too much.

Michelle Trenum kept coming back to the same question.

“If you’re that worked up,” she says, “then what are you doing letting your kid out there in the first place?

Read more about her son Austin who killed himself days after a concussion during a high school football game and their journey since Austin’s death.


Identifying CTE before death?

June 28, 2012

Currently, the only way to officially diagnose CTE is after death.  Scientists at UCLA may have found a way to identify the presence of the Tau protein (which accumulates in the brain after head injuries and causes CTE) before an autopsy is needed….


The question, after a decade of brain-slicing autopsies, is when any of this will help players before they’re dead. Doctors can’t just crack open living patients’ skulls and lop off slices of their brains to stick under a microscope.

But new research at UCLA is using a cutting-edge biomarker that can attach itself to tau protein tangles so that they show up on PET scans of living subjects. Dr. Gary Small is currently running a pilot study on retired NFL players, imaging their brains in place. If he is successful, his work would reorient the science of head injuries around saving lives instead of merely contextualising deaths.

Link to full article

Drug trial started that may help grow brain cells impacted by CTE

June 28, 2012

Interesting news given everything I’ve been learning about CTE.  One of the treatment issues with CTE is that it is not related specifically to the chemicals in the brain (dopamine, serotonin, etc.)  In most cases of depression and mood disorders our brain chemicals can be affected by stimulants and depressansts.  For people like my brother antidepressants had little effect… because the depression was likely exacerbated by brain damage and not purely a chemical imbalance.  This drug focuses on rebuilding brain cells and not on brain chemical regulation.


“We are pleased to begin testing the safety of NSI-189 in depression patients,” said Karl Johe, PhD, Neuralstem’s Board of Directors and Chief Scientific Officer. “We believe it could help patients who suffer from depression via a new mechanism that does not seek to modulate brain chemistry, but rather stimulates new neuron growth in the hippocampus and increases hippocampal volume, thereby potentially addressing the problem at the source.”

In addition to ALS, the company is also targeting major central nervous system conditions with its cell therapy platform, including spinal cord injury, ischemic spastic paraplegia and chronic stroke. The company has submitted an IND (Investigational New Drug) application to the FDA for a Phase I safety trial in chronic spinal cord injury.

Neuralstem also has the ability to generate stable human neural stem cell lines suitable for the systematic screening of large chemical libraries. Through this proprietary screening technology, Neuralstem has discovered and patented compounds that may stimulate the brain’s capacity to generate new neurons, possibly reversing the pathologies of some central nervous system conditions. The company has received approval from the FDA to conduct a Phase Ib safety trial evaluating NSI-189, its first neurogenic small molecule compound, for the treatment of major depressive disorder (MDD). Additional indications could include chronic traumatic encephalopathy (CTE), Alzheimer’s disease, anxiety, and post-traumatic stress disorder (PTSD).

link to full article

Weekend Warriors, Police Officers, Second Impacts often fatal

June 22, 2012


Although the recent news flurries about concussions have centered around the NFL after the suicide of Junior Seau on May 2nd, the vast majority of concussion victims are ordinary citizens.  Actually, the number one cause of sports-related head injuries is bike riding.  Although concussions are most often associated with athletes, law enforcement officers are certainly not immune to concussions and/or chronic traumatic encephalopathy in the line of duty or in training.  Take the example of Norfolk Police recruit John Kohn.   According to reports, Kohn was first punched in the face by a police trainer during training; he reported the incident to his wife and classmates, complaining of a headache.  Two days later he sustained additional head blows by another student and the instructor during a ground fighting session until he blacked out. Paramedics responded and he was flown to a hospital where he underwent brain surgery.  He remained in critical condition until he was taken off life support on December 18th, 2010. Doctors determined that the cause of death was due to multiple brain injuries (second-impact syndrome).  Whether he had reported his injuries to his superiors is under debate (and key to a pending lawsuit by his widowed wife).

The Norfolk Police have made changes in their training; they now ban intentional head strikes and require additional training for instructors and recruits in identifying and reporting possible injuries.  The NFL has also repeatedly made changes related to their head injury protocol.  But is it enough?  How much damage has already been done?  Do you know enough about concussions; not only as a LEO, but as a weekend warrior?  What about chronic traumatic encephalopathy?

Read the full article.

Please view our Wish List, sign the Registry, join the Discussion Boards…

June 17, 2012

Our goal in creating this site was to establish and build a virtual community of support.

Please view our WISH LIST, sign our REGISTRY, and join in our DISCUSSION BOARDS.



Press Release – HeadsUp! CTE Formed in Honor of Sean O’Malley, Ole Miss Rebel #99 and the Cardio Coach

June 12, 2012


Heads Up! CTE ( is formed to support former athletes and their families dealing with Chronic Traumatic Encephalopathy

June 12, 2012

Following the suicide of former All SEC Ole Miss Dean’s List football player Sean O’Malley (#99) this past March, Sean’s family and friends started an organization called Heads Up! CTE to bring awareness about Chronic Traumatic Encephalopathy (CTE) to other former athletes and their families.

Colleen O’Malley, Sean’s sister, her husband Jeff Weber, and her parents Dr. Charles ‘Chuck’ and Nancy O’Malley decided to form Heads Up! CTE after realizing that Sean suffered from CTE and not clinical depression and ADHD.  Sean started seeing medical specialists in his 20s following some changes in memory and attention and was diagnosed with ADHD.  In his 30s, his family started watching his behavior shift as he went from being a world famous motivational fitness coach known as the Cardio Coach ( to a recluse.  As he approached his late 30s many interventions were made to bring Sean to the best medical professionals who tragically never questioned Sean’s history with head injuries or linked his changes in behavior, memory and mood to CTE. Instead they diagnosed him with clinical depression and put him on pharmaceuticals which Sean complained never worked. Just before Sean’s 41st birthday, Sean took his own life.

Following the funeral Colleen, Jeff and Sean’s former college girlfriend and fellow Ole Miss athlete, now Mental Health Specialist and Licensed Clinical Social Worker, Angela Brignole English, started comparing notes and stories about Sean’s behavior changes.  It became apparent Sean had what was becoming publicly known as the Pro Football Players disease: CTE.  As others in Sean’s circle started hearing about his death, they too began sharing information and stories confirming Sean was experiencing all of the symptoms of CTE and not clinical depression.

Colleen captured her and Angela’s research, as well as articles about CTE sent in from dozens of Sean’s fans and friends in a blog site which is now at  This site houses the latest news, resources, treatment options, discussion boards and a registry for CTE victims to ‘sign in’ and find support.  Together with Angela and Dr. Michelle Reillo, founder of the Hyperbaric Treatment Association (HTA) Heads Up! CTE is bringing awareness, diagnostic tools, and resources to other forgotten athletes, their families and their communities through workshops, races, webinars, social networking, and other events.  The goal is not only to provide awareness but funding and treatment options for all CTE victims so that no one else has to lose their loved ones to this tragic disease.

The Link Between Traumatic Brain Injuries (TBI) and Depression

June 12, 2012


Wondering what’s causing your depression? Have any concussions or other forms of brain injury in your past? Well, if you do it might explain the way you’re feeling, because having a brain injury, even a minor one, greatly increases your risks of depression – even years after the fact.

Traumatic Brain Injury

Traumatic brain injury (TBI) occurs when you get hit, bumped, jolted or pierced severely enough to cause some temporary or permanent change to brain functioning.

  • TBIs can range in severity from mild to severe and can be fatal
  • Mild TBIs cause a momentary loss of consciousness or a temporary change in mental functioning, such as feelings of wooziness, seeing stars, headaches, short term memory loss or feeling confused. About 75% of TBIs are concussions or other forms of mild brain injury. People rarely seek medical care for a mild TBI.
  • More serious TBIs may involve longer periods of unconsciousness or coma and or more severe amnesia

Other TBI facts:

  • Symptoms of TBI may occur right away or they may not emerge until days or even weeks following the injury. Some common TBI symptoms include headaches, difficulties with memory or clear thinking, mood changes, a ringing in the ears, changes to sleeping habits and feelings of fatigue. These symptoms can persist for a long while and TBI can cause depression or anxiety, even years after the fact.
  • Traffic accidents cause about half of all TBIs. Other common causes include getting hit in the head with a hard object, banging your head on the ground or against another hard object or being in close proximity to an explosion (a frequent cause of military TBIs)

Free Concussion Treatments for Retired/Former Athletes

June 12, 2012

EXCERPTS from Press Release:


Former NFL players reveal the role of HGH and Testosterone in their successful treatment of concussion related symptoms

The P.A.S.T. Retired Athlete Medical Group that provides fully integrated medical care to retired athletes including NFL, NBA, NHL and MLB players announced today the launch of a comprehensive concussion treatment program that will be made available to all retired NFL players and other former athletes. The program is solely focused on the reduction of symptoms and restoration of quality of life.

The initial phase of the new program can be started by a player from home. The program is tailored to each specific person and utilizes a unique combination of diagnostics, advanced blood work, specialized diets, supplements, therapy, player to player support systems and in some cases hormone replacement therapy when medically indicated. The program was designed so a player could initially engage with the program from home. Some players will even have the opportunity to have a phlebotomist do their initial blood draws for the program testing at their homes.

Many players who have used these types of protocols have seen significant improvement in symptoms such as energy, depression, mood swings, sleep disturbances, chronic pain and more. They have experienced relief of symptoms and restoration of quality of life.

For some former NFL players HGH (Human Growth Hormone) and Testosterone have played a significant and successful role in treating their concussion related symptoms. The new program incorporates extensive testing of hormone levels and Hormone Replacement Therapy when medically indicated.

note from HeadsUp! CTE – we will be researching these treatment options to learn more.  Felt this was too important to not share ASAP.

Does the NFL ‘Glorify’ Violent Hits?

June 10, 2012


In December of the 2010 season, NFL Commissioner Roger Goodell announced stricter discipline, including suspensions, for illegal hits to the head or neck. Last December, the league began using athletic trainers in the press box to spot players wobbled by potential concussions and alert medical staff on the sideline.

“It took decades for the NFL to admit that there was a problem and sixteen years (1994 to 2010) to admit that its information was false and inaccurate,” says the complaint. “The NFL’s conduct in this regard is willful and wanton and exhibits a reckless disregard for the safety of its players and the public at large.”

In addition to the NFL and NFL Properties (the league’s marketing arm), the defendants in the master complaint include Riddell, official helmet of the NFL. It had been named in some of the individual suits.

“At the time the helmets were designed, manufactured, sold, and distributed by the Riddell … the helmets were defective in design, unreasonably dangerous, and unsafe for their intended purpose,” says the master complaint.

The complaint also alleges the league glorified violent hits through NFL Films productions, claiming the league used them to promote “the most violent aspects of NFL football and to urge players at every level of the game to disregard the results of violent head impacts.”

(link to full article)

Canadians Bringing Awareness, Research and Funding to Canadian Sports Concussion Project

June 9, 2012


Charles Tator, CM, MD, PhD, FRCSC FACS, neurosurgeon at Toronto Western Hospital, professor at the University of Toronto, founder of ThinkFirst Canada, will be celebrated and thanked for the decades of work he has done on brain injuries and the mysterious effects of concussion.

There is likely no one who knows more about hockey concussions than Tator, and yet he would be first to admit he knows next to nothing at all.

“We know only the tip of the iceberg,” he says. “There remains a huge amount we do not know.”

Tator hopes to change that with an ambitious plan to raise, ultimately, $25-million for his Canadian Sports Concussion Project that is under way at the Krembil Neuroscience Centre at Toronto Western. On the Monday following his USA Hockey award, he will meet with a new advisory group – which includes Hockey Hall of Famer Ken Dryden and Boston Bruins star Marc Savard, who is still suffering the effects of concussion – and plans will be laid to turn the project into the leading source for brain injury research in the country, just as Boston University has been leading the way in the United States.

Already Canadian neuroscientists at Western have studied the brains of four deceased former CFL players – two found to have suffered from chronic traumatic encephalopathy (CTE), two without but showing signs of Parkinson’s disease and amyotrophic lateral sclerosis (ALS or Lou Gehrig’s disease) – and have under study two more donated autopsied brains of Canadian football players.

“There will now be a Canadian counterpart to the work being done in Boston,” Tator says.

At the moment, he says, “We don’t have an accurate way of even diagnosing concussion.”

Link between concussions and suicide/depression in football players

June 9, 2012


In a Jan. 18 (2007) article, University of Pittsburgh neuropathologist Bennet Omalu, MD, claimed that the successive concussions experienced by former Philadelphia Eagles defensive back Andre Waters led to his depression and eventual suicide in November. He also reported that Waters’ brain had degenerated to resemble that of an 85-year-old man with pathology similar to early Alzheimer disease (AD). Waters was only 44 when he died.

Girls’ Lacrosse Team Voluntarily Wears Rugby Helmets

June 9, 2012

The Bullis School girls’ lacrosse team has voluntarily decided to wear rugby helmets for the 2012 season in an effort to provide added protection against concussions.

Smash Cap

June 9, 2012

Students invent Smash Cap which uses wireless technology to detect if a concussion occurred, its intensity, and what action should be taken.

NFL Law Suit – 3365 plaintiffs vs. NFL

June 9, 2012

(AP News) — Lawyers for former NFL players plan to file a single lawsuit Thursday consolidating scores of complaints brought against the league in the past year accusing the NFL of concealing information linking football-related head injuries to permanent neurological problems.

According to an AP review of 81 lawsuits filed through May 25, the plaintiffs include 2,138 players who say the NFL did not do enough to inform them about the dangers of head injuries. The total number of plaintiffs in those cases is 3,356, which includes players, spouses and other relatives or representatives.

Some of the plaintiffs are named in more than one complaint, but the AP count does not include duplicated names in the total.

(link to full article)

Symptom Survey

June 9, 2012

Please review the Symptoms page for more specifics about CTE and common symptoms being reported in medical and scientific literature.  Below is a survey we created to learn more about the symptoms we are experiencing and observing.  With my brother he had many of these symptoms which appeared slowly over time and then began to consume him.

NFL Hid Link Between Football-Related Head Trauma and Permanent Brain Injuries, Lawsuit Says

June 8, 2012


Plaintiffs hope to hold the league responsible for caring for players suffering from dementia, Alzheimer’s diseases and other neurological conditions. “I want this game to be around, to be a great sport, a sport that my own boys will be able to play and enjoy all the benefits I believe that football has,” former Eagles and Patriots running back Kevin Turner, now suffering from amyotrophic lateral sclerosis, said in the suit.  “Let’s face it and be honest, I feel like the NFL has over the past decades — at least until ’08 or ’09 — kind of turned a blind eye to the seriousness of not only concussions … but the cumulative effect of (hits) and how these retired players are having so much difficulty in getting along in their daily lives.”

The lawsuit accuses the NFL of “mythologizing” violence through the media, including its own NFL Films branch. The lawsuit also makes claims of negligence and intentional misconduct in its response to headaches, dizziness and dementia reported by ex-players. “After voluntarily assuming a duty to investigate, study, and truthfully report to the public and NFL players, including the Plaintiffs, the medical risks associated with MTBI in football, the NFL instead produced industry-funded, biased, and falsified research that falsely claimed that concussive and sub-concussive head impacts in football do not present serious, life-altering risks,” the complaint says, according to the AP.

The league has rebuffed similar accusations in the past. Currently, the NFL provides a series of medical benefits to help former players, including the 88 Plan, which provides funding to treat dementia, Alzheimer’s disease and ALS.

Full article: