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Category Archives: Brain Injury Treatment
Spreading depolarizations trigger early brain injury after subarachnoid hemorrhage, researchers find – Medical Xpress
Posted: September 6, 2017 at 5:45 pm
The study of Hartings and colleagues found that bleeding onto the surface of the brain (a subarachnoid clot) can directly cause the death (infarct) of the affected brain gray matter the cerebral cortex. Progression to death is mediated by repetitive brain tsunamis (cortical spreading depolarizations), shown here by blue waves and arrows, that spread through the cortex. Brain tsunamis reduce blood supply to the brain (cortical spreading ischemia) and impair brain function, resulting in flatline (terminal depolarization) as the tissue dies. Brain tsunamis were first described in 1944 by Aristides Leo and today are measured in patients with electrodes placed on the brain surface. Credit: Illustration by Tonya Hines, Mayfield Clinic
The phrase “time is brain” could take on new meaning when applied to the treatment of subarachnoid hemorrhage, a type of bleeding stroke, thanks to research partially funded by the Mayfield Education & Research Foundation and the United States government.
Subarachnoid hemorrhage, caused by the rupture of a brain aneurysm, affects an estimated 10 to 15 of every 100,000 individuals each year. An international team of researchers has established that the blood from this type of hemorrhage launches deadly “brain tsunamis” within hours, leading to permanent brain damage. This damage, known as infarction, occurs in the cerebral cortex near the hemorrhage and can cause permanent disability and in some cases death.
Brain tsunamis, scientifically known as cortical spreading depolarizations, are travelling waves of brain dysfunction that spread out from an injury site and contribute to worse outcomes in patients. They affect patients who suffer trauma to the brain as well as those who suffer various types of stroke. In subarachnoid hemorrhage, blood from a ruptured aneurysm or shredded artery pools in the space between the arachnoid membrane and the brain itself.
A team of researchers led by Principal Investigator Jed Hartings, PhD, Research Associate Professor in the Department of Neurosurgery at the University of Cincinnati, used a novel animal model to study what happens immediately after a subarachnoid hemorrhage. The team also monitored 23 patients who were surgically treated for subarachnoid hemorrhage at hospital locations of Charit University Medicine in Berlin. Monitoring was accomplished by placing electrode strips on the surface of the brains of animal models as well as patients.
The team’s findings of secondary damage within 6 hours were published online today in the journal Brain.
“We found that patients who suffered brain damage in their frontal lobes were more likely to have experienced spreading depolarizations than those who had no damage,” Dr. Hartings says. “The animal studies showed that these pathological changes can arise as a direct result of the blood accumulation in the grooves of the brain that the presence of blood in the wrong place is toxic to the brain.”
In the past, researchers have focused primarily on delayed complicationssuch as the narrowing of major cerebral arteries known as vasospasm that occur 5 to 14 days after subarachnoid hemorrhage. Those complications account for only a minority of deaths (13 percent), however; the majority of deaths from subarachnoid hemorrhage (86 percent) occur in the early hours and days after an aneurysm rupture occurs. The present study sheds new light on these early events and suggests that they may be preventable.
“This is the first evidence that brain tsunamis are a clinical marker, and mechanism, of early brain injury,” Dr. Hartings says. “As such, they provide us with an opportunity to pursue therapeutic interventions that could improve outcomes for patients. By treating or preventing brain tsunamis, we could potentially stop many victims of bleeding stroke from suffering additional, often catastrophic, brain damage.”
The early damage caused by subarachnoid hemorrhage has been underappreciated, Hartings says, because it often cannot be observed with routine CT brain imaging. “There has also been a sense that early damage could not be prevented, but perhaps that perception is starting to change.”
Looking ahead, the researchers propose the investigation in animal models of therapies that target spreading depolarizations in an effort to interrupt or prevent secondary injury processes.
When a brain injury occurs, nerve cells in the brain (which act like batteries by storing electrical and chemical energy) malfunction and effectively short-circuit. Because all nerve cells in the brain are connected, this depolarization causes all the neighboring cells to short-circuit as well; this subsequent leakage of precious electrical charge moves like a tsunami through the brain, with the potential to cause additional permanent tissue damage.
To document the cascade of events that immediately follows subarachnoid hemorrhage, the research team used a novel swine model, whose brain, with grooves and fissures, more closely resembles the human brain than previously studied rodent models. The researchers found that clots that quickly formed in the grooves of the swine brain mirrored the results in the human brain; in both situations, the clots caused repetitive spreading depolarizations and lesions (infarcts) in the cerebral cortex shortly after an aneurysm rupture and subarachnoid hemorrhage.
The study’s collaborating scientists and clinicians are members of COSBID (Co-Operative Studies on Brain Injury Depolarizations.
Explore further: Subarachnoid hemorrhage and the need for expert treatment
More information: Ayata C, Lauritzen M. Spreading Depression, Spreading Depolarizations, and the CerebralVasculature. Physiological Reviews. 2015;95(3):953-93.
Baechli H, Behzad M, Schreckenberger M, Buchholz HG, Heimann A, Kempski O, et al. Blood constituents trigger brain swelling, tissue death, and reduction of glucose metabolism early after acute subdural hematoma in rats. J Cereb Blood Flow Metab. 2010;30(3):576-85.
Bosche B, Graf R, Ernestus RI, Dohmen C, Reithmeier T, Brinker G, et al. Recurrent spreading depolarizations after subarachnoid hemorrhage decreases oxygen availability in human cerebral cortex. Ann Neurol. 2010;67(5):607-17.
Bretz JS, von Dincklage F, Woitzik J, Winkler MKL, Major S, Dreier JP, et al. The Hijdra scale has a significant prognostic value for the functional outcome of Fisher grade 3 patients with subarachnoid hemorrhage. Clin Neuroradiol. 2016:in press
Hartings JA. Spreading depolarization monitoring in neurocritical care of acute brain injury. Curr Opin Crit Care. 2017;23(2):94-102.
Hartings JA, Shuttleworth CW, Kirov SA, Ayata C, Hinzman JM, Foreman B, et al. Thecontinuum of spreading depolarizations in acute cortical lesion development: Examining Leao’s legacy. J Cereb Blood Flow Metab. 2017;37(5):1571-94.
Posted: at 5:45 pm
On March 19, 2012, Brian Grundtner fell 50 feet during an airborne training jump, sustaining multiple broken bones and a traumatic brain injury.
Four years later, the former special operations staff sergeant overcame his TBI to graduate from the Carlson School of Management with his Masters of Business Administration.
Grundtner, a native of White Bear Lake, Minnesota, said he chose the University for its military veterans MBA program.
I think the biggest factor for me was the veterans initiative and the emphasis on integrating veterans into the whole MBA program, Grundtner said. It really helped with the transition out of the military and into the civilian world.
Retired naval officer Charles Altman, the MBA military veterans program director, said financial assistance make the University’s one of the best programs for veterans.
Twenty percent of Carlsons full-time MBA students are veterans and all of them get scholarships, Altman said. Those who complete the program have a 100 percent employment rate after graduation.
In a lot of cases what veterans need more than anything else is a leg up this funding provides them that, Altman said, adding he spent time getting to know Grundtner while he was a student.
Dave Hopkins, a professor in Carlson, said Grundtner stood out in his classes as a personable student and hard worker.
I knew that he had some challenges in overcoming some injuries, but it didnt impact him with me in any way, Hopkins said. He was a great asset to the program.
Veterans, especially those struggling with trauma and injuries, often struggle to return and translate their military and leadership skills to civilian life, Altman said.
Grundtners accident was the start of a long recovery process.
I was knocked out after I landed. When I woke up, my eyes didnt work right away, he said.
Though he didnt immediately realize the extent of the brain injury, he said he began to notice difficulties with everyday tasks.
I would be reading a book and the words would all just turn into a bunch of letters, Grundtner said. Or if I was sitting in front of a computer screen for more than 30 minutes I would just get an immense headache.
He received treatment for over a year at a concussion care clinic at Fort Bragg in North Carolina, where he focused on vision therapy and concentration. As a result, he said he hasnt had a migraine since June 2013.
Grundtner now works in software sales at IBM and spreads the word about TBIs with the Defense and Veterans Brain Injury Center’s initiative A Head for the Future.
Hopefully my participation in this program can connect me with other TBI victims or concussion victims, Grundtner said, adding he wants to encourage veterans to pursue recovery and careers.
Read the original here:
Carlson offers veteran a new start after brain injury – Minnesota Daily
Posted: at 5:45 pm
Photographee.eu/ShutterstockSome of the early symptoms of Alzheimers Disease are the same as those of depression, including apathy and irritability. As a result, many patients with Alzheimers Disease (AD) are prescribed antidepressant medications. A group of scientists from the University of Eastern Finland were concerned that this practice could be increasing the risk of head and brain injuries among AD patients. Heres why:
First, AD is a disease associated primarily with the elderly. Second, antidepressant use among the elderly is associated with an increased risk of falling down. Finally, falling down is the number one cause of head and brain injuries in the elderly (compare this to younger people, who more often experience head injuries as a result of motor vehicle, sports, and other accidents).
Since there were no existing studies investigating the risk of head or brain injuries associated with antidepressant use, let alone studies that focused on the AD patients or even the elderly, the Finnish scientists took it upon themselves to investigate whether antidepressant use is associated not only with an increased risk of falling, but also with an increased risk of head and brain injury in Alzheimers patients. What they found is that the use of antidepressants by AD patients is, in fact, associated with a higher risk of head injuries.
Their study, the results of which were recently published in the journal, Alzheimers Research & Therapy, included 32,700 AD patients living in nursing homes, 10,910 of whom used antidepressants and 21,820 of whom did not. Each of the people who used antidepressant medication was matched with two users who did not, based on age, gender, and time since AD-diagnosis. Head and brain injuries were recorded, numbers were crunched, and the association became clear: the risk of head injury goes up immediately upon starting the medication and continues to be elevated for up to two years.
Antidepressant use has been previously associated with an increased risk of falls, the study authors report, but our novel findings indicate that they are associated with severe injurious falls, i.e., those resulting in head or brain injuries among persons with Alzheimers disease.
Future studies will be required to confirm the association between antidepressant use and head and brain injuries, and the study authors would like to conduct further research to determine whether the risk of head injury increases in all elderly people who use antidepressant medications, as opposed to just elderly AD patients.
For now, the study authors recommend that the use of antidepressants be carefully considered in those with AD, and in the elderly in general. Instead, practitioners may prescribe anti-psychotics, which have been the traditional treatment of choice for the behavioral and psychological symptoms of dementia. The use of anti-psychotics comes with its own set of risks, including life-threatening brain events such as stroke and hemorrhage. However, knowing the risks of the available treatments for AD will allow for more-informed prescribing.
Even if you dont have AD, your meds might be causing you problems. For example, here are some warning signs youre taking too many prescription drugs.
Posted: at 5:45 pm
This article was originally published on The Conversation, an independent and nonprofit source of news, analysis and commentary from academic experts. Disclosure information is available on the original site.
Author: Kathryn Schneider, Assistant Professor, Clinician Scientist (Physiotherapist), Faculty of Kinesiology, University of Calgary
Recognize, remove, rest and recover before returning to sport. Those are key points about sport-related concussion stated in the 5th International Consensus Statement on Concussion in Sport.
The Canadian Guidelines on Concussion in Sport have been developed based on this statement and were recently released by Parachute Canada, a charitable organization focused on injury prevention, and its expert advisory group.
The good news is that most people who suffer a concussion will recover in the initial days and weeks following injury. However, some will have ongoing symptoms. While concussions may occur in sport, there are many benefits to physical activity and sport participation for both youth and adults.
I am a physiotherapist and researcher (assistant professor and clinician scientist) at the Sport Injury Prevention Research Centre, Faculty of Kinesiology, University of Calgary. My research focuses on the prevention and treatment of sport-related concussion in children, youth and adults, with special emphasis on the role of the neck and balance systems.
A concussion is a type of a brain injury that occurs following a trauma to the head or body. Symptoms can come on immediately or may take hours to gradually evolve. The most common symptom following concussion is a headache. However, a number of other symptoms such as dizziness, nausea, fatigue, difficulty with concentration, neck pain and other complaints may also occur. Lying motionless, clutching the head, being slow to get up, wobbling and appearing dazed are some of the observable signs.
In the event that a concussion may have occurred, it is important that the player is removed from the activity and has follow-up medical evaluation as soon as possible. A tool called the Concussion Recognition Tool 5 (CRT5) has been developed by the Concussion in Sport Group and is meant to help coaches, officials, parents and players recognize the signs of concussion.
How are concussions treated?
All individuals with a suspected concussion should see a health care professional with knowledge of concussion. The typical treatment is a short period of rest (24 to 48 hours, both mental and physical) followed by a gradual return to the typical activities that are done throughout the day.
Following this, individuals may slowly increase their activity level using a graduated return-to-school strategy and return-to-sport strategy.
The return-to-school strategy includes steps to gradually increase the amount of mental activity prior to returning to school.
The return-to-sport strategy includes a series of steps that are performed sequentially, with each step taking a minimum of 24 hours. These include light aerobic exercise, sport-specific exercises, non-contact training drills and full practice prior to returning to play or sport.
These two strategies can be performed simultaneously under the supervision of a health care professional. They take approximately one week to complete as long as the person with the concussion does not have any recurrence of symptoms. It is recommended that individuals return to school prior to returning to sport. Medical clearance should be obtained prior to returning to sport.
Most people get better in the initial days to weeks following a concussion. However, for those who have ongoing symptoms and difficulties, there are some treatments that have been shown to help.
My research has found that people with ongoing headaches, neck pain and/or dizziness and balance problems who are treated with physiotherapy techniques aimed at treating the neck and balance systems are more likely to be medically cleared to return to sport in eight weeks.
There is also some research that low-level aerobic exercise may be beneficial following a concussion. Our research in this area is ongoing and we currently have a number of studies that are evaluating different types of treatments to help with recovery.
Is there any way to prevent a concussion?
The best way to minimize the impact of concussions is to prevent them. To do this, we first need to understand who is at the greatest risk.
Research has shown that individuals who have had a previous concussion, who play games (as opposed to practice) and engage in contact sports all increase the risk of concussion.
Many different sport associations are working to use research to inform rule changes to decrease the risk of concussion, including rules to disallow bodychecking in youth ice hockey nationally, in leagues for 11-to-12-year-olds (based on research led by Carolyn Emery).
Another focus of my research program is to evaluate different pre-training strategies that may be used to prevent concussions.
Concussions in sport are an area of much discussion. It is imperative that individuals with a suspected concussion are removed from play until they can be medically evaluated and do not return until they are cleared to do so.
At this time, the literature on the long-term consequences of exposure to head trauma is inconsistent. Thus, more research is required to answer these important questions.
The good news is that most people recover well following a concussion when managed appropriately. Awareness of the signs and symptoms of concussion, and appropriate initial management when a concussion may have occurred, are of utmost importance.
This article was originally published on The Conversation. Disclosure information is available on the original site. Read the original article:
Posted: September 4, 2017 at 7:44 pm
A father who was left severely brain damaged after Royal Perth Hospital doctors failed to act in a timely way to diagnose and treat his bacterial meningitis has been awarded more than $7million in damages.
In a judgment handed down in the District Court last week, Judge Patrick ONeal ruled Peter Panagoulias was entitled to the multimillion-dollar payout after finding failures by hospital staff left him with disabilities that are properly described as tragic.
Mr Panagoulias was diagnosed with a brain tumour in 2005 and, while it was benign, he had surgery in 2006 to have it removed.
According to the judgment, the first surgery, at Mount Hospital, was unsuccessful in removing the entire tumour and Mr Panagoulias went under the knife again in September 2007.
During that procedure, neurosurgeon Emil Popovic nicked Mr Panagoulias carotid artery, causing a major bleed, and the surgery was abandoned.
The bleed was treated, but over the next three weeks Mr Panagoulias, then 40, complained of headaches and a constant discharge from his nose.
On October 6, he presented to the RPH emergency department with a severe headache.
Despite doctors suspecting he may have had bacterial meningitis, Mr Panagoulias was not given antibiotics until 7 hours later.
By then, he had suffered an irreversible brain injury.
Mr Panagoulias now requires supportive care for the rest of his life and lives in a nursing home interstate.
At a trial in March, lawyers for his wife Fiona accused RPH doctors of failing to exercise proper care in diagnosing and treating the infection.
Judge ONeal ruled in the couples favour, finding RPH staff breached the duty owed to the plaintiff by failing to act in a timely way to diagnose and treat the bacterial meningitis.
I find that it should have been apparent to any reasonably competent medical practitioner, given the plaintiffs history and presentation … that there was a high probability that he was facing a serious medical emergency and that harm would occur if care were not taken in his treatment, he said.
Judge ONeal awarded Mr Panagoulias more than $4.5 million in damages for his future needs and $425,000 in general damages for pain, suffering and the loss of amenities of life.
He also awarded more than $2 million in special damages and took account of his future earnings as an accountant.
The breach of duty by the staff … transcended mere negligence, the judgment said.
Mrs Panagoulias also tried to sue Dr Popovic, who died in 2011, alleging he failed to advise his patient to seek emergency treatment for what turned out to be a symptom of meningitis.
However, Judge ONeal dismissed the claim.
Lawyer Karen Jarman, speaking on behalf of Mrs Panagoulias yesterday, said that the case was never about finances but a pursuit to ensure that hospitals are answerable for their errors.
For Mrs Panagoulias, this fight is about ensuring that no family has to endure the tragic outcome that they will continue to live through, Ms Jarman said.
An East Metropolitan Health Service spokeswoman said: Given the complexity of the case, the judgment is currently being reviewed … and therefore it is inappropriate to comment.
See more here:
$7m payout for brain damage – The West Australian
Posted: at 7:44 pm
One man’s story
Fed up with the unrelenting pain and feeling despondent about his life, Gerald Duvall stuck the loaded gun into his mouth and pulled the trigger.The arthritis in his knees and feet, the herniated disc in his back and the effects of a brain injury had become overwhelming. After serving 10 years in the Army that included five deployments to the Middle East, Duvall came back home to Monroe and battled feelings of worthlessness and depression. And he drank.But the alcohol mixing with the 20-some prescription pills he ingested daily led to blackouts that were confusing and frightening. And when he did pull that trigger, the gun simply clicked. It was a misfire. And it was also a sign.I said to myself: What am I doing? Duvall recalled. It meant that I needed to be here.During one of his blackouts, he drove and was pulled over. Arrested for drunken driving, Duvall could have become another statistic, another defendant in the criminal justice system. Instead, he entered Veterans Treatment Court. And after a year of counseling, treatment and supervision Duvall is now much more content and has remained sober for the past six months.They really do care, Duvall said. They treat you like a human being. It probably saved my life.Duvall, 37, said he was worried at first about sharing his story publicly but decided that by doing so, he might make a difference in another veterans life. He said he knows there are others out there like him who had to battle substance abuse, despondency and feelings of worthlessness that accompany many servicemen and women who return from the war and find themselves in transition to civilian life without direction, order or even reasons for living. He fought all those demons before receiving the help he needed.You start feeling worthless, he said. The anger was probably the worst.As a member of the 82nd Airborne, Duvall made 67 jumps during his decade in the Army. All those landings from the jumps damaged his back and injured his feet and knees. He said he lost three inches from his height.Every year from 2002 to 2010 was spent in Iraq or Afghanistan. And while he didnt see much combat, the nearby explosions were ever present and threatening. Back home, he was diagnosed with Post Traumatic Stress Disorder (PTSD).But the booze mixing with the pills led to serious problems, such as the blackouts where he couldnt remember arguments or even fights.I definitely had drinking issues, he said.After his arrest in 2016, Duvall entered the Veterans Court program and began intense therapy that involved four trips a week to the VA hospital in Ann Arbor. He said those involved with the program are veterans so they could relate to his issues. He understood that he needed help and realized that he either must complete the program or be sent to jail.He had a relapse while in the program that involved alcohol, anger and guns. Again, it was a wakeup call and hes remained on course ever since. Duvall completed the requirements and after a year he graduated from the program. Now he wants to become a mentor and join the countys Veterans Court to help others.Im all about helping veterans, Duvall said. Im definitely a success story.These days Duvall and his wife of six years, Melissa (theyve been together 12 years), are hoping to close on a house in Jackson where the couple and their four children can live hopefully in peace. He said he is happy and focuses on being a better husband and father.He is confident he will remain sober and stay out of trouble. He says hes doing well and is ready to move forward while enjoying life, something he believes might not have been possible without Veterans Court. His legal issues also have been resolved.If I didnt go through Veterans Court I would be in prison or dead by now, Duvall said. And I do know I have friends if I need to talk.
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Veterans Court ‘saved my life’ – Monroe Evening News
Posted: September 3, 2017 at 8:44 am
Some of the diplomats hurt in a mystery sonic harassment attack on the US embassy in Cuba suffered brain injuries or permanent hearing loss, their staff association said on Friday.
Washington recently said at least 16 embassy employees were injured in a series of incidents in Havana that began last year, but officials have not revealed the extent of the injuries.
Now, the American Foreign Service Association the labor union representing US diplomatic and international aid personnel has been able to speak to 10 of those who received treatment.
Diagnoses include mild traumatic brain injury and permanent hearing loss, with such additional symptoms as loss of balance, severe headaches, cognitive disruption and brain swelling, it said.
The State Department has called the attacks unprecedented and has warned Havana it is responsible for the safety of envoys working on its soil without saying who it believes was behind them.
Staff members at the US mission, which was reopened as a full embassy in 2015 after a half-century Cold War breakdown in diplomatic relations began reporting sick last year.
US officials have told reporters they believe some kind of sonic device was used to covertly undermine the envoys health.
Some of the 16 staff who were hurt were evacuated to Miami for treatment in US hospitals, while others were cared for by American doctors who travelled to Havana to work at the embassy.
Separately, Canada has said one of its diplomats posted to Havana is also being treated for hearing loss.
In May, the US ordered two Cuban diplomats to leave their own recently reopened embassy in Washington and return to Havana, without publicly saying why.
It is now known that Washington had alerted the Cuban government to what Havana dubs the alleged incidents as far back as February 17.
But US officials made no public complaint until just last month when US Secretary of State Rex Tillerson warned that Cuba must help investigate and prevent further attacks.
Tillersons spokeswoman Heather Nauert said on Thursday last week that the incidents do now appear to have ended, but that investigations are ongoing to find the culprits.
This latest attack is regrettably only the latest example of the many threats facing members of the foreign service as they serve their country abroad, the staff association said.
The body urged the US government to do everything possible to provide appropriate care for those affected, and to work to ensure that these incidents cease and are not repeated.
Posted: at 8:44 am
Courtesy of Astrocyte Pharmaceuticals
Imagine a pill that could make all the NFL’s concussion problems go away.
Imagine a treatmentor a battery of treatments, therapies and toolsthat eradicates CTE and makes concussions only slightly more mysterious and threatening than sprained ankles.
Imagine equipment that provides swift, precise diagnoses, pills that provide immediate relief and speedy recovery and medications that can actually repair the damage that causes long-term brain damage.
Imagine wonder drugs that improve (and sometimes save) the lives of not only football players, but also of military veterans, crash victims, stroke victims, opioid addicts and perhaps even those with Alzheimer’s disease.
It sounds like science fiction. Or a Roger Goodell daydream. But the race to find just such treatments is already underway, and significant progress has already been made.
The “concussion pill” may be coming soon.
“This is coming in 2025 if all goes well,” Dr. William Korinek,the CEO of Astrocyte Pharmaceuticals, said of a drug that turbocharges the brain’s ability to heal its own damage.
Dr. Kun Ping Lu, who’s working on a medication that destroys the compounds that cause brain damage, isn’t quite that optimistic but said, “I hope it should be here in 10 years.”
From the sound of it, there appears to be hope for concussion victims and CTE sufferers on the not-too-distant horizon.
But right now, that hope spends most of its time running through laboratory mazes.
Of Mice and Men
If you give a mouse enough concussions, it becomes antisocial, reckless…or even suicidal.
The search for a concussion pill is largely in the “mouse model” phase right now. Researchers expose rodents to tiny (for us) pressure blasts which cause major (for them) damage, then study the results, either anatomically through autopsies or behaviorally through experiments.
It turns out that mice with traumatic brain injuries (TBIs) suffer many of the same symptoms which now plague former football players.
Dr. Korinek described one such test. A so-called “teenage” mouse is given five concussions within a week. The mouse is then allowed to grow to its equivalent of middle age. Then the “Three Chamber Social Interaction Test” is applied. A “stranger” mouse is placed in one section of a three-chambered apparatus, behind a glass plate. The afflicted mouse then has its run of the other two chambers.
“Mice are social creatures,” Dr. Korinek explained. “The mouse is going to see that stranger mouse and check it out.”
A healthy mouse will spend twice as much time in the chamber next to the stranger as in the third, isolated chamber. But the mouse who suffered multiple concussions in its youth behaves differently.
“They may check out the other mouse, but they end up spending equal amounts of time between the two chambers,” Dr. Korinek explained. “They don’t have the same curiosity or interaction that you see in a normal mouse who has not been injured.”
The human analog is both obvious and chilling. Former football players with CTE symptoms, most notably Junior Seau, are known to isolate themselves socially, which only compounds their physical and emotional struggles.
Dr. Lu, a professor of medicine at Harvard University, described an even more revealing experiment, one in which mice with TBI are placed in mazes that contain high-elevation, exposed “arms.”
“Mice are afraid of heights and afraid of open space,” Dr. Lu explained. “Because in nature, mice in the open are going to get eaten by eagles.”
Healthy mice instinctively avoid the high, open portions of the maze, just as they avoid scurrying across the middle of your kitchen floor in broad daylight. But the afflicted mice behave very differently.
“After traumatic injury, it doesn’t matter. Open arm? Closed arm? They just do it, because they don’t sense that by going out into the open arm there’s a risk.”
Again, the human analog is clear and frightening. Individuals who suffer CTE symptoms often engage in compulsive, sometimes dangerous behavior, throw themselves through glass doors, even attempt or commit suicide: all signs of the brain’s risk-assessment software going haywire.
But these lab mice are not suffering in vain.
Dr. Korinek’s research has resulted in a medication that prevents the onset of anti-social mouse behavior. “If we treat these mice within a half-hour of their concussions, then look at them again when they are “40 year olds,” they don’t have those symptoms,” he explained.
Dr. Lu and researchers at Harvard have created a different treatment: an antibody that keeps mice from running blithely beneath the potential path of a hungry raptor. “After the antibody treatment, they’re back to normal. When they see the open arm, they don’t go out there.”
These drugs aren’t just anesthetizing the mice or masking symptoms. While the drugs work differently, they each perform a similar function: they make the brain better at healing itself.
Good Guys, Bad Guys, Helpers and Pruners
Most of the breakthroughs that led to the current race for a concussion drug occurred in the last decade or so. Neurologists still grapple with misunderstandings and emerging research. Luckily, they have come up with some analogies and metaphors to keep the rest of us from becoming hopelessly lost.
“Think of it like the police,” Dr. Lu explained of his research. “The toxic proteins are the bad guys. The antibody can arrest them and not allow them to do damage to the brain.”
Dr. Lu was studying the telltale “tangles” in the brains of Alzheimer’s patients, the same evidence of severe damage found in the brains of CTE sufferers, and in his research discovered a toxic form of the P-tau protein labeled cis P-tau which becomes prevalent in the brain before the tangles develop. Regular P-tau is helpful to brain function. The toxic cis P-tau is devastating.
If, as Dr. Lu suggested, you think of the brain as a highway, the cis P-tau “basically makes the highway lane collapse, jams the traffic,” Dr. Lu said. “Cars cannot move, the signal cannot transmit and neurons die.”
So Dr. Lu developed an antibody that keeps mice from wanting to become eagle food. It’s similar in principle to a vaccine, “arresting” the “bad guy” without damaging anything else. Because cis P-tau may be one of the agents which cause Alzheimer’s disease, the antibody may have applications that range far beyond treating ex-football players or sufferers of TBI.
Dr. Korinek, meanwhile, focused his research on astrocyte cells, which for decades were assumed to be gap-fillers or insulators for the brain’s message-carrying neurons. As it turns out, astrocytes are more than just the rubber around the wires. “The astrocyte has really emerged as the caretaker cell in the brain,” he explained.
“It’s the astrocytes that are helping clear away the signal to make sure it keeps functioning well. It’s turning over or pruning 20 percent of the synapses at all times.”
Given plenty of time, astrocytes can prune away the damage suffered during a concussion. But repeated concussions overtax the astrocytes at the cellular level. Dr. Korinek’s treatment that makes mice sociable again “helps energize the caretaker cells, recharging their batteries so they are able to function again.”
Both treatments show exceptional promise so far. But mouse tau protein is not human tau protein, and the human brain is so much more complex than a rodent brain that there is no guarantee that what works in a laboratory maze will automatically work for a football player coping with CTE. Dr. Korinek’s team will soon ramp up experiments to larger mammals, while Dr. Lu synthesizes a human version of the protein that’s suitable for human pilot studies.
But while two teams of researchers perform miracles with mice, others are developing treatments which have gotten resultsfor some well-known former players.
Jamie Dukes, former NFL lineman and NFL Network personality turned founder and CEO of Pro-IV, rattles off a laundry list of retired football players and other athletes currently using his treatment. It’s a collection of Hall of Famers and Mt. Rushmore types, as well as more recent retirees like Michael Vick, who has gone on record endorsing the Pro-IV DripFusion therapy.
“When I got my first infusion, it was great,” Vick said in a radio interviewon behalf of Pro-IV. “I played a flag football game that night. No stretching or anything. And I felt like I was 22 again.”
Dukes isn’t shy about boasting what he believes his treatment could do. “This is the lone solution to the opioid epidemic as it stands today,” he said.
According to Dukes and his chief neurological surgeon, Dr. Kevin Jackson, a version of the same treatment that makes Vick feel rejuvenated can be used to mitigate the effects of concussions. And this treatment is not 10 years away or trapped in the rat race of mouse mazes. “Before the end of the year, we should have three FDA drug indications for some of our therapies: two for chronic pain and one for our acute concussion protocol,” Dukes said.
Dr. Jackson based the treatment on studies which showed that concussions have an impact on micronutrient levels in the brain.
“Magnesium levels fall in the brain after a head injury, regardless of the severity,” he explained. “Urinary zinc increases fourteenfold. We know that there are minerals associated with brain function that change after a head injury.”
The Pro-IV treatment is essentially a “cocktail” of substances that aim to rebalance those micronutrients, with some anti-inflammatories and non-opioid pain relievers mixed in to treat immediate symptoms. All of the individual ingredients are FDA approved; hence, retired players like Vick can already receive the treatment.
Because Pro-IV reached the market before undergoing full clinical testing, both Dukes and Dr. Jackson are quick to point out that endorsements like Vick’s are purely anecdotal evidence of the treatment’s efficacy.
There’s one clinical study underway with retired football players, another with the Veterans Administration.
Right now, Pro-IV is an intravenous treatment: patients are infused with the substance via a saline bag. It’s inconvenient, not covered by insurance and involves needles. Dr. Jackson hopes to reconfigure the treatment into a pill, patch or nasal spray. He also acknowledges the need to determine ideal dosages and do all of the other nitty-gritty medical work that stands between making Michael Vick feel young again and creating a medicine that insurance carriers will cover and can be safely administered to a high school athlete who suffers a concussion.
But Dukes said that there is no shortage of former NFL players willing to take an IV full of substances that haven’t officially cleared all of the clinical and governmental hurdles. Such is the fear and urgency among ex-players, due both to the ailments so many of them face and the studies which increasingly link those ailments to CTE.
Of course, there’s another substance with well-known mood-altering effects which is also in the midst of a broad but not-quite clinical trial among both NFL players and the public at large.
The Whole Entire Plant
Nate Jackson played six NFL seasons filled with major and minor injuries, yet he needs no traditional medications to get through his days.
“I use cannabis when I am in pain but otherwise lead a medication-free lifestyle,” he said.
To be clear: when Jackson says “cannabis,” he is not referring to some specialized strain of marijuana biologically engineered to treat pain symptoms without the other lava-lamp-and-cookie-binge effects.
“When I say cannabis, I mean the whole entire plant,” he said. “Cannabis, marijuana, weed: It’s all the same plant.”
Jackson is abreast of the research which separates the cannabidiol (CBD) substance in hemp plants, which may have both anti-inflammatory and neuroprotective elements, from tetrahydrocannabinol (THC), the substance that gives marijuana its notorious kick. But in Jackson’s estimation, both CBD and THC may have a role in healing the many ailments ex-football players suffer from. “But we’re learning that feeling might be helping to heal your body.”
The University of Miami received a $16 million grant last October to determine whether CBD mixed with an “NMDA antagonist” (a type of anesthetic) can be used as an effective treatment for concussion and traumatic brain injury.
The Miami study is expected to last five years. Researchers are not yet ready to report any significant results.
“We’re doing some basic testing of the properties of the compound in model (i.e. mice) format, in preparation for designing something for human use,” Miami researcher Dr. Michael Hoffer said.
Dr. Hoffer’s team has had more immediate success with a concussion diagnostic tool: virtual reality goggles that monitor eye movement when a potentially concussed patient tracks a series of moving targets across a virtual field. The goggles have a 95 percent diagnostic rate, according to Dr. Hoffer, and can be used to gauge the severity of the injury and provide feedback during treatment/recuperation.
Diagnostic goggles don’t sound like much of a consolation prize when pursuing a marijuana-based concussion cure. But the devices could help take the guesswork out of a medical diagnosis still fraught with subjective elements.
“The pill can’t be effective for concussions if you can’t diagnose one,” Dr. Hoffer said.
While marijuana is regularly prescribed by physicians in some states, its federal status as a Schedule 1 narcotic has slowed study of its medical value..
But Jackson is among many who feel that “weed” could hold the key to a better quality of life for many ex-players.
“I played six years. Chances are that my brain has been altered by the game. But I am not feeling symptomatic. Why am I not? If I do, when will it happen? Did the cannabis I used when I was playing help protect my brain? Is it helping me now? A lot of us say it is helping, but that’s just our hunches. We don’t know for sure.”
“You have athletes who are hurting, who have pain and brain damage, and this plant seems to be something that can help them all.”
Urgency and Skepticism
Astrocytes. Tau proteins. Micronutrients. CBD and THC. It can be a lot to sift through. Especially for someone who already fears or is starting to cope with the symptoms of traumatic brain injuries or CTE.
Some potential remedies sound too good to be true. Jackson said that former players aren’t always equipped to tell the difference between a treatment with real scientific merit and a patent medicine that is formulated solely to separate them from their remaining NFL dollars.
“Football players have fallen prey to all kinds of silly science,” Jackson said. “Snake-oil salesmen, not just with medicine but with business practices, all of that stuff. We have a very bad real-world sense. We’ve been coddled. We tend to not look really skeptically at people when they offer to help us.”
It’s hard to be skeptical when you’re desperate for a cure. Dr. Lu says that he receives calls and emails from people with TBI affliction who are ready to take his protein antibody. They don’t care that it’s not human protein; they’ll take their chances with mouse protein. Naturally, they are turned down. “That’s not ethical and probably will not be effective,” Dr. Lu deadpanned.
“Right now, there are no treatments,” Dukes said. “What they consider a treatment is: Go in a room, turn the lights off, have everybody whisper to you. That’s treatment by definition.”
Most current CTE research (as well as the money that fuels it) still focuses on prevention and diagnostic tools like the University of Miami goggles. But “we’re going to quickly be at the point where we know concussions are very bad and we can diagnose them accurately, but you can’t do anything about it,” according to Dr. Korinek.
Soliciting NFL dollars to conduct research, meanwhile, can be a double-edged sword. “They just don’t have the credibility in the area,” Dukes said, “because when they do anything, it’s always viewed as being tainted.”
The most encouraging component of concussion “pill” research right now is not any particular breakthrough; it’s the fact that so many researchers are making so much progress along so many vectors.
Not all of the treatments will ultimately prove to be safe and effective. But more potential solutions increase the chances of success. “You need a lot of shots on goal in this space,” Dr. Korinek said.
Players will be waiting, even if it takes years for those shots to reach the net. “Whenever that comes, it will be helpful,” Nate Jackson said. “Guys will hold on. They are all very tough, very stoic.”
“We will lose some guys, but we will have some guys who will really benefit from it.”
Researchers, meanwhile, are well aware that while their first priority is saving lives, they may also be saving a sport.
“I have two sons who are eight and 10,” said Dr. Korinek. “I told them they can’t play football until dad’s medicine’s on the market.”
Mike Tanier covers theNFLfor Bleacher Report. Follow him on Twitter:@MikeTanier.
Posted: August 31, 2017 at 11:49 am
LONDON — Since announcing a $100 million commitment to concussion research last year, the NFL has funded just one study examining chronic traumatic encephalopathy, or CTE, the brain disease that has shaken pro football. But that study isn’t focused on football players.
It’s focused on jockeys.
The project, run out of a four-story brick building in northwest London, aims to find out why high concussion rates in horse racing don’t translate into “deteriorating brain function in later life,” a question that many scientists believe has little to do with football. The study is led by an Australian researcher who once described American coverage of CTE as “carry-on and hoo-hah” and a British doctor whose concussion presentations sometimes have included flippant jokes and video of tumbling jockeys set to slapstick music. At one presentation, the widow of a CTE victim, a former British soccer star, was so offended she stormed out of the room.
The jockey project is part of the NFL’s latest effort to stake out a powerful role in research that holds the potential of its own undoing.
Last September, the NFL pledged $100 million, doubling down on its previous commitment as one of the largest funders of concussion research in the United States. The league and its advisers say the money will go toward the prevention, diagnosis and treatment of head injuries. But after years of donating to outside entities — an approach that league officials said was designed to keep the research independent — the NFL has taken the science in-house and under its control.
“I would view it just as if any giant corporation was doing internal research,” said Stefan Duma, a concussion researcher who is the interim director for Virginia Tech’s Institute for Critical Technology and Applied Science. “This is internal research that the NFL controls.”
The NFL’s “Play Smart, Play Safe” initiative was announced as the league came under heavy criticism for trying to influence a CTE study to be administered by the National Institutes of Health. The league made a $30 million “unrestricted gift” to the NIH in 2012, but the partnership blew up after the controversy and will end today with more than half of the money unused.
Among its goals, “Play Smart, Play Safe” aims to spend more than half of the $100 million to create a safer helmet as a means of reducing concussions. A similar NFL project failed more than a decade ago, and many scientists believe the focus on helmets avoids the primary issue: CTE. At the same time, the NFL has joined global sports organizations — including the NHL and World Rugby — in pushing back against mounting evidence that sports-related head trauma can lead to CTE, a disease associated with dementia, memory loss and depression.
The NFL declined to make any of its health officials available for comment. When declining one specific request, a league spokesman cited previous “unfair” treatment by ESPN’s Outside the Lines. In the past, the league has said it is guided by player health and safety. Several NFL-affiliated researchers have suggested that scientists such as Boston University’s Dr. Ann McKee and Robert Stern, aided by the media, have oversold their findings, sowing unwarranted hysteria over the risks of playing football and other contact sports. McKee, a neuropathologist, announced in July that out of the 111 brains of former NFL players she has examined, 110 had CTE.
The prevalence of CTE among former NFL players — and the rate at which they develop the disease — has not been established. Because McKee and other researchers rely on individual case studies, some experts, particularly those affiliated with the NFL and other sports organizations, say the underlying cause of CTE is still unknown and might be due to other factors, such as alcohol or steroids. As well, McKee acknowledges her data set is skewed, making it difficult to assess the true prevalence of the disease.
When “Play Smart, Play Safe” was announced last year, NFL commissioner Roger Goodell acknowledged “there is skepticism about our work in this area” and pledged that “both the process and the results” would be made public. Much of the NFL-sponsored research remains unclear, including whether any NFL money will be spent on studying CTE or other long-term neurodegenerative diseases in football players.
As part of the initiative, the league formed the NFL Scientific Advisory Board, a committee that will recommend how the NFL should spend $40 million it set aside for scientific research. Retired Gen. Peter W. Chiarelli, the chairman, said the board will receive research applications this fall. He said it was too early to specify the focus of that research but stressed the importance that it “provide something of use to the league and the players.” Chiarelli said he believes it’s imperative to develop methods for diagnosing concussions quickly and accurately to improve treatment. But he said he has received no guidance from the NFL that would prevent the board from recommending any study or research area, including one that focuses on CTE.
Chiarelli said he is convinced that the NFL is committed to addressing brain injuries.
“They’re spending more money than anybody else,” he said, adding that money is no substitute for a true collaboration that involves researchers, academic institutions and industry coming together to solve the myriad problems around traumatic brain injuries.
The NFL has not disclosed how much it has invested in the London jockey project, which is being conducted by a nonprofit organization called the International Concussion & Head Injury Research Foundation. The project studied jockeys for the first 12 months but has been expanded to include athletes from other impact sports, according to the ICHIRF website.
When the league announced “Play Smart, Play Safe,” it touted the partnership under the headline “How Horse Racing Research May Help Make Football Safer.” The foundation lists its sponsors as the NFL and Godolphin, a global horse racing syndicate. The ICHIRF’s Scientific Committee includes NFL advisers, including Dr. Allen Sills, the league’s chief medical officer, and Dr. Richard Ellenbogen, co-chairman of the NFL’s Head, Neck and Spine Committee. The committee also includes one neuropathologist, Dr. Rudy Castellani, the director of the Center for Neuropathology at Western Michigan University and an expert witness for the NHL in a class-action lawsuit alleging the league hid the dangers of concussions and long-term issues. Castellani also has raised questions about the significance of McKee’s findings.
One of the researchers leading the study, Dr. Michael Turner, said in a 2015 interview with Sky Sports: “What interested [the NFL] about our project is the fact that we have this cohort of jockeys, retired jockeys in their 50s, 60s and 70s who suffered a lot of concussions when they were younger and don’t appear to have any long-term ill effects of it.”
Several concussion researchers told Outside the Lines they were unaware of any notable studies examining the incidence of long-term brain issues in jockeys.
Asked about concerns that the NFL might try to use the results to argue the league doesn’t have a brain injury problem, Turner said in the Sky Sports interview: “The research has to stand on its own, and the fact that we get some money from the NFL is not a big worry. They’re not breathing down our neck. They are merely providing funds for a research project that is of interest to them, as I suspect it is to a number of different organizations.”
Turner declined to be interviewed by Outside the Lines for this story.
The Injured Jockeys Fund, a UK-based organization that provides support to hurt jockeys and their families, also is funding some of the ICHIRF research and providing subjects.
“This is a peer-reviewed research project,” said Brough Scott, an ICHIRF board member who was a successful jockey and is the chairman of the board of trustees of the IJF. “We don’t know what will turn up. If it turns up something that is very serious, we’ll have to face up to it.”
Several concussion experts reached by Outside the Lines doubted that equestrian sports were an appropriate vehicle to draw conclusions about long-term mental illness in football players. Comparing jockeys with NFL players is like “comparing apples and pears; you’re talking about completely different population groups, completely different physiologies,” said Angus Hunter, an exercise physiologist and concussion researcher at the University of Stirling in Scotland whose recent study with neuropsychologist Magdalena Ietswaart suggested repetitive blows from heading a soccer ball can lead to notable changes in brain function.
“With a jockey on a horse, if he comes off, there’s a high chance of getting a concussion, but he’s not impacting the brain hundreds of times in a race,” said Dr. Willie Stewart, a neuropathologist at Queen Elizabeth University Hospital. “If you have a rugby player, perhaps there’s a lower instance of concussion, but there’s a difference in brain impacts that are causing the repetitive subconcussive insults hundreds, maybe thousands of times a season.”
Stewart has become a leading figure overseas in CTE research. He worked with McKee and several other neuropathologists on a $12 million NIH study — funded by the NFL through the NIH — that defined the pathology of the disease and noted that “thus far, this pathology has only been found in individuals exposed to brain trauma, typically multiple episodes.”
During a 2013 concussion conference in England, after a Stewart presentation, Turner jokingly described Stewart as the “Attila the Hun of Concussion,” according to several people who attended the event.
Turner is the ICHIRF’s medical director and formerly served as chief medical officer for the British Racing Authority. He has raised doubts about the connection between head trauma and CTE at a time when research continues to mount connecting the two.
“When you look at the CTE research, you find that actually a lot of the people who they have seen don’t have CTE on their brain, and that normal people who’ve never had a concussion, and have stacked shelves in a supermarket all their lives, do have CTE,” Turner said in a 2016 interview with Neurology Central, a website that provides content related to neuroscience. “So we don’t really understand the relationship between CTE and concussion.”
Dr. Daniel Perl, a leading neuropathologist and a professor at the Uniformed Services University of the Health Sciences, said Turner’s view is inaccurate.
“The overwhelming majority of cases of CTE have been in the context of multiple trauma,” Perl said.
Turner has sometimes added humor to his concussion presentations, according to people who have attended his sessions. During several presentations, Turner has played a highlight reel of jockeys falling off horses, set to a soundtrack of Benny Hill-like music, according to people who have seen the video.
To researchers accustomed to lengthy and often turgid scientific analysis, the presentations can be lively and refreshing. But many people say they have been offended by Turner’s speeches. One is Dawn Astle, the daughter of former British soccer great Jeff Astle. Known as “The King,” Astle’s father starred in the 1960s and 1970s for West Bromwich Albion and played for England in the 1970 World Cup. He died at 59 in 2002 from a neurodegenerative disease that left him unrecognizable to family and friends.
During his playing career, Astle was known for his brilliant ability to propel the ball with his head. Stewart later diagnosed Astle as the first soccer player to have CTE.
Astle’s daughter is a former narcotics investigator and has become an advocate for pushing research of CTE in soccer players and for the families of former players. She encountered Turner during a 2016 concussion conference at Twickenham in suburban London but said she left his presentation early based on what she saw.
“You can be a jokester and an entertainer, but not when you’re talking about people’s lives,” she said. “I just felt like he was trivializing it and he was laughing.”
Astle said she finds it hard to believe that Turner is in charge of a project to investigate CTE in sports.
“I wouldn’t let him anywhere near that,” she said. “No way, never in a million years. That’s probably why [the NFL] has chosen him, to discredit everybody and say, ‘Oh, it doesn’t exist.'”
Turner’s primary co-researcher with the ICHIRF has expressed doubts about CTE.
“Just think for a moment: If the [CTE] story is true, and it’s related to the jarring or constant hits, we should see an epidemic of jockeys with problems, and we don’t,” Paul McCrory, the chairman of the ICHIRF’s Scientific Committee, said during a presentation last year titled, “The Concussion ‘Crisis’: Media Myths and Medicine.” “That’s a clue that the CTE story really has a few questions that we don’t understand yet.”
McCrory, an associate professor at the Florey Institute of Neuroscience & Mental Health in Australia who has been a consultant to at least 10 sports organizations, including the International Olympic Committee and FIFA, declined through an ICHIRF spokesman to be interviewed for this story. But in papers and public presentations, he has questioned whether CTE is a real problem. He is an expert witness for the NHL in its concussion case.
“It’s fair to say there is increasing skepticism around the world as to whether this condition actually exists or not, and that might seem very strange and provocative to say, because if you listen to the media, you get a very different story,” McCrory said at a 2013 FIFA conference, according to audio aired on Background Briefing, an Australian public affairs program. “The media will tell you that it’s a conspiracy, that every hit causes brain damage. None of that’s true.”
During a 2016 presentation, McCrory claimed that 20 percent of McKee’s subjects had “no actual pathology,” and he suggested that what she calls CTE in many cases might be another disease, such as Alzheimer’s. In the same presentation, after noting that four subjects reportedly suffered from headaches, McCrory told his audience: “Well, I get a headache, maybe I’ve got CTE.” He also cited a study that he said showed NFL players were 60 percent less likely to commit suicide than the general population and said, “So you could argue that playing NFL football actually protects you from mental health issues.”
In explaining why McKee and others could be wrong about CTE, McCrory talked about how tau, the protein that causes CTE by strangling neurons in a definable pattern, is simply “part of the aging process” and present in all brains.
“Oh, my God, that’s just ludicrous and misleading. It’s embarrassing that a neurologist would say that,” said Steven DeKosky, the deputy director of the McKnight Brain Institute at the University of Florida and one of the world’s leading Alzheimer’s experts, when McCrory’s statement was read to him.
CTE is different from Alzheimer’s and other diseases, with a distinctly identifiable pattern of tau, DeKosky said. Dismissing the disease by claiming that this pathological form and location of tau is part of normal aging is “like saying if you have a nose with two nostrils you must be a serial killer, because all serial killers have two nostrils. That’s a facile comment about tau, but absolutely wrong.”
McKee, of Boston University, said the campaign to raise doubts about CTE is “getting more brutal. It’s getting more personal.”
The NHL went to court in 2015 to try to obtain McKee’s records, including autopsy photos, a demand that “threatens the foundation on which science thrives,” McKee wrote in response. In one filing, the NHL compared McKee’s work to that of a widely discredited British scientist who linked autism to vaccines.
An April “consensus statement” signed by researchers affiliated with more than a dozen sports organizations — including eight with the NFL, plus Turner and McCrory — called the connection between sports-related head trauma and CTE “unknown.”?In March 2016, Jeff Miller, the NFL’s top health and safety officer, acknowledged a link between head trauma and CTE — the first time a senior NFL official conceded the connection. But since then, the league has seemed to suggest the relationship is still unclear.
“I don’t understand how [sports organizations] could let certain potential conflicts get in the way of their view of things that are relatively straightforward to the people who truly understand this type of disease,” said Boston University’s Stern, who asserts that the link between head trauma and CTE is “incredibly clear.”
The NFL-NIH partnership blew up after the NIH selected a group led by Stern to run a $16 million CTE study that was to be funded by the league.
So far, the NFL has announced just two projects from its $100 million “Play Smart, Play Safe” campaign, totaling $210,000. “It’s going to take 500 years to distribute this money” at this rate, said one concussion researcher, who requested anonymity in the hopes of still receiving funding from the league.
Much of the pledged money — $60 million — is being spent on an “engineering road map” that encourages technological innovation to reduce head trauma.
The NFL believes that building better helmets — and making the technology available to the public — will reduce concussions. The idea is not new: The league embarked on a similar strategy in 1994, conducting internal research with the goal of creating a concussion-resistant super helmet. Back then, Dr. Robert Cantu, a renowned concussion expert, warned that the NFL’s helmet strategy was naive. Today, he believes focusing on helmets remains misguided.
“The majority of that $100 million — $60 million — is going to technology, and ‘technology’ is a nice word to say ‘better helmet,'” said Cantu, a clinical professor of neurosurgery at Boston University who has studied concussions for four decades and is a consultant with the NFL. “They’re hoping they can come up with a better helmet that will largely make the problem go away. Helmets can obviously make it better, but no, realistically, it’s the violent shaking of the brain, the rapid movement of the head. And the masses involved of individuals colliding with their heads and other body parts is just too great. They could probably get it better, but I don’t think the helmet will ever solve the issue.”
Jeff Crandall, a highly regarded researcher who is the director of the Center for Applied Biomechanics at University of Virginia and the principal scientist at Biocore, a Charlottesville firm, is overseeing the NFL’s latest helmet project. The league declined to make Crandall available. During a meeting launching the “engineering road map” last year, Joel Stitzel, chair of the Department of Biomedical Engineering at Wake Forest Baptist Medical Center, said his group suggested making the study of so-called “subconcussive impacts” a potential research priority for the NFL.
“I said, ‘We feel like it’s important to study long-term impacts: What are the long-term consequences of subconcussive impacts'” on the brain, Stitzel recalled in an interview. “And the answer was: ‘That’s not in the scope of what we are trying to evaluate.'”
Stitzel praised Crandall as an excellent researcher but said he believes there are limits to what the NFL-funded project can accomplish. “I feel like there’s diminishing returns on helmets,” he said.
Some scientists wonder whether the NFL is skirting the larger issue — CTE and other long-term brain issues — by focusing most of its resources on helmets. In this way, they said, the league can keep debate focused around concussions instead of repetitive head trauma, which McKee and many others believe is the primary cause of CTE.
As part of its $100 million pledge, the NFL committed $40 million to scientific research. Chiarelli, the chairman of the Scientific Advisory Board, said in an interview that his committee will evaluate proposals this fall and make recommendations to the NFL. Chiarelli said the advisory board was thinking big to maximize the impact of the research: “I think it’s fair to say we want to avoid funding a whole bunch of science fair projects.”
Chiarelli, after retiring as vice chief of staff of the U.S. Army, became CEO of One Mind, a Seattle-based nonprofit research organization, to help find solutions to an epidemic of traumatic brain injuries that he first saw in the military. Chiarelli said the NFL research will provide benefits not only for football but also for veterans and the 2.8 million people who, according to the Centers for Disease Control, report to emergency rooms with concussion symptoms each year.
Chiarelli said the advisory board will make its recommendations independently, but the NFL will have the final say.
“What we’re going to do is make recommendations,” he said. “They’re going to decide how to spend their money.”
See the rest here:
NFL retakes control of brain research as touted alliance ends – ABC News
Risk of post-traumatic epilepsy after severe head injury in patients with at least one seizure – Dove Medical Press
Posted: at 11:49 am
Video abstract presented by Wei Chen.
Wei Chen,1 Ming-De Li,2 Gui-Fang Wang,1 Xia-Feng Yang,1 Lin Liu,1 Fan-Gang Meng3
1Department of Neurology, Liaocheng Peoples Hospital, Liaocheng, 2Department of Neurosurgery, The Peoples Hospital in Ling Cheng District, DeZhou, Shandong, 3Department of Functional Neurosurgery, Beijing Neurosurgical Institute, Capital Medical University, Beijing, China
Background: To explore the incidence and risk factors, including type of seizures for post-traumatic epilepsy (PTE) after severe traumatic brain injury (TBI).Subjects and methods: This was a retrospective follow-up study of patients discharged from Liaocheng Peoples Hospital between March 2011 and June 2015 with a diagnosis of post-traumatic seizures. Risk factors for PTE were evaluated in 68 inpatients by using KaplanMeier curves and the Cox model.Results: Complete clinical information was available for 68 patients. A total of 54 cases (79.4%) were diagnosed as presenting with PTE, occurring from 10 days to 179 months after severe TBI. Nineteen out of 54 cases (35.2%) had been defined as PTE within the first 6 months after the trauma, 17 cases (31.5%) within 712 months, 8 cases (14.8%) within 1324 months, 2 cases (3.7%) within 2536 months, and 8 cases (14.8%) within 37179 months after the TBI. The KaplanMeier curves demonstrated that simple partial seizures, surgical treatment, and onset of seizures occurring within 6 months after injury were associated with PTE.Conclusions: The Cox model indicated that, for patients aged >34 years at the time of injury, the PTE risk was 2.55 times greater than for those aged 34 years. In addition, simple partial seizures, surgical treatment and onset of seizures occurring within 6 months after injury were significant risk factors for the development of PTE.
Keywords: post-traumatic epilepsy, risk factor, post-traumatic seizure
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