A Yale football player quits to save his brain

Andrew Grinde was not just another football player. As a running back at C.M. Russell High School in Great Falls, Mont., he rushed for 2,180 yards and 20 touchdowns in 2014, leading the Rustlers to the state title game, and was named Montana’s Gatorade Football Player of the Year.

Swift, stocky, powerful and fearless, he outran some defenders and bowled others over. His highlight video is worth watching. Find it at www.hudl.com/profile/2376679/Andrew-Grinde.

With a 4.0 grade-point average, Grinde (rhymes with Lindy) was recruited by Ivy League schools, as well as the University of Montana and Montana State. He headed off to Yale before deciding to take a year off from school and football. His return to the gridiron the next summer merited a story in the Great Falls Tribune. “I miss it, for sure,” he told the reporter. “I love playing.”

Grinde, who goes by Drew, returned to Yale and in his first collegiate game carried the ball four times for 45 yards and a touchdown. But in practice the following week, he had a bruising collision while pass blocking against a 240-pound linebacker.

The next morning in class, another student asked him whether he was drunk. “I was slurring my words,” he told me by phone from New Haven, Conn. He immediately went to the university health clinic and found he’d suffered a concussion.

He sat out for a week and a half, but when he resumed practice, something was wrong. “I got very lightheaded and could barely feel my legs,” he recalls. That was enough. “I cleaned out my locker that night.”

Grinde had been playing tackle football since he was in fifth grade. He had been a high school star. But he could no longer accept the risk to his cognitive function and mental health.

Even before that episode, he had begun to worry. His brother was studying neuroscience at the University of Montana and told him that playing football “was probably the worst thing you could do for yourself as an adolescent.”

He wasn’t deterred, but every time he got hit in practice, he would think about concussions and the cumulative damage he might be doing to his brain. “Playing football wasn’t the same,” he says.

He had cause for concern. The Centers for Disease Control and Prevention notes that chronic traumatic encephalopathy, an incurable degenerative brain disease, “is believed to be caused in part by exposure to repetitive head impacts, including concussions as well as subconcussive trauma.” It adds, “The greatest risk factor for CTE is the number of years of exposure to repeated head or brain injuries.”

Football involves exactly that sort of exposure. A Boston University study found CTE in 110 of 111 brains of deceased NFL players. Of the 53 brains from college players who didn’t make the NFL, the disease was detected in 48 of them — 91 percent.

Scientists examined the brains that the Mayo Clinic had preserved from patients with neurodegenerative disorders. CTE was present in 1 in 3 of those who had played contact sports — and none of those who hadn’t.

The NFL resisted the evidence about the effects of the game but eventually had to admit reality. It reached a settlement covering some 20,000 former players, which is expected to cost $1 billion. The NCAA also is facing lawsuits and last summer settled one from a University of Texas player’s widow who sought $1 million.

Grinde spent years meting out and incurring hits to the head. He now has to live with the fear of developing symptoms of CTE.

Last year, I wrote a column arguing that Harvard and Yale, as two of the world’s premier educational institutions, should stop subjecting their undergraduates to the danger of irreversible damage to their excellent brains. Grinde read it recently and emailed to tell me, “This article aligns with what I have been preaching to many of my peers at Yale, both football players and non-players.” That email led to our conversation.

The Ivy League has tried to curb the problem by banning tackling during in-season practices and moving kickoffs from the 35- to the 40-yard line to increase the number of touchbacks. But these changes can’t fix a sport designed to batter brains. Reducing the number of alligators in a lake wouldn’t make it safe for swimming.

Drew Grinde has ensured that one Yale undergraduate won’t be at high risk of brain damage every fall Saturday. Yale could ensure that none are.

By Steve Chapman for the Chicago Tribune

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A talk with Mike Adamle about his Rise Above Project, a joint initiative with the Concussion Legacy Foundation

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Dr. Cole and Steve Kashul talk with Mike Adamle about his Rise Above Project, a joint initiative with the Concussion Legacy Foundation and their mission to create a supportive network of resources for all affected by CTE.

As you may know, Mike Adamle has been diagnosed with dementia, andImage result for mike adamle chicago bears doctors believe it is CTE due to all his successful years on the football field. We are now one family among many fighting this terrible neurodegenerative disease. When Mike bravely told his story, he received hundreds of messages from people of all walks of life struggling with the same symptoms of TBI and looking for help, answers and support.

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An Athletic Trainer’s Role in Helping Prevent, Assess and Care for a Concussed Athlete

An Athletic Trainer’s Role in Helping Prevent, Assess and Care for a Concussed Athlete

By ATI Physical Therapy

The role a certified athletic trainer (ATC) plays in preventing, assessing and caring for a concussed athlete is critical to an athlete’s return to play and overall health. The ATC is often the first line of defense in injury prevention, which is why it is essential they be on the field, court or arena where injuries may occur.

As injury cases such as concussions, continue to evolve, keeping up with these progressions requires a careful adaption in the injury assessment treatment methods. To that, ATI Physical Therapy ATCs put a great deal of effort in staying up on monitoring symptoms along with implementing return-to-learn and return-to-play protocols.

As far as preparation, ATI’s Sports Medicine division is pivotal in ensuring all ATCs are prepared to assess concussions by requiring them to undergo very specific and rigorous training programs that educate the team on current protocols prior to each sport’s season.

Concussion prevention

In an effort to thwart off a concussion, an ATC will continually work with their athletes to provide effective guidance and education on techniques that help with avoiding concussion-enabling situations. In doing this, an ATC will often follow these protocols:

  • Ensure: Ensure that the players’ equipment is properly fitted and the playing environment is safe to participate.
  • Educate: Educate coaches, parents and players before the start of the season about the inherent risks of a concussion and the proper protocol if a suspected head injury has occurred.
  • Assist: Assist with strengthening programs that increase neck stability, which can decrease the frequency of concussions.

Assessing concussions

In recent years, return-to-play success rates have steadily enjoyed a healthy uptick. With much help from researchers such as Dr. Ellen Shanley and her work on youth football tackling and training methods, concussion assessment protocols and tools continue to improve.

There are several neurocognitive systems that most high schools utilize, which obtain a baseline test score pre-participation. As a result, if a concussion is suspected, a post-injury test can be performed immediately. In some states, there have also been increased state regulations that all high schools must follow. This has significantly improved the landscape of how concussions are assessed and treated.

Concussion care

When an athlete is diagnosed with a concussion, an ATC is responsible for looking after the concussed athlete on a daily basis. Since every concussion is unique, each case must be handled individually to ensure the athlete is completing all the required steps and is ready to safely return to action. Traditionally, the stages ATI ATCs follow for a concussed athlete include:

  • Education: It is crucial that a concussed athlete and their family be educated on the injury, what to expect and the next steps that need to be taken.
  • Contact: After an injury occurs, the ATC is the point-person for any orders from the athlete’s primary physician for school modifications and symptom monitoring. When an athlete is symptom-free, the ATC will be in contact with their doctor, school nurse, coaches and athletic director to ensure the athlete advances on to the return-to-learn phase.
  • Return-to-Learn: The return-to-learn phase is when the athlete returns to school and begins working their way back to a full academic workload.  The ATC coordinates with the school nurses and councilors to ensure the athletes are following physician protocols and safely moving through the return-to-learn phases.
  • Return-to-Play:  Once the return-to-learn protocol is completed, the ATC completes a return-to-play progression with the athlete. This is a step-by-step process that ramps the athlete’s activity level back up. This serves to ensure that the athlete’s symptoms don’t return and that the athlete has the confidence to return to their sport they love to play.

Spotting a concussion

Spotting a concussion is a method that continues to change in the concussion climate, which is why it is crucial an ATC be current on assessment protocols. In its most common form, a concussion can be spotted when an athletic trainer sees a head-to-head collision. A head-to-head collision is the most obvious indicator of a concussion and almost always warrants a thorough evaluation provided by an ATC. It is important to note that not all concussions come from head-to-head collisions.  Some concussions come from rapid rotation or can even be caused from smaller repetitive blows to the head.

Assessing a concussion in the initial stages can be tricky, which is why it is important athletic trainers connect with their athletes and get to know them personally to spot any unusual changes in their mood and energy. An ATC will put themselves in the middle of the athletes during timeouts and breaks during practices and games to get a read on their athletes, look at their eyes and ensure that everyone is healthy to participate. While an ATC serves as the team’s primary concussion-spotter, it is also important that athletes and coaches catch potential head injuries and communicate any potential issues with the team’s ATC.

Recently, new technology in helmets can measure and notify athletic trainers when a high velocity impact has occurred. Athletes wearing this technology in their helmets will be pulled from practice or competition if an impact hard enough to cause damage occurs or if several smaller impacts have occurred and the sum of those collisions crosses a certain threshold.

Playing with a concussion

An athlete who continues to play with a concussion is putting their health at an increased risk of sustaining something called second impact syndrome.  Second impact syndrome is a condition that occurs when a second instance or injury occurs to the brain that has already sustained an injury that was not completed healed.  This has the potential to be a life-altering injury. This is why ATCs are so vital in preventing, assessing and caring for head injuries.  If you or someone you know has recently experienced a head injury, get it checked out right away. Stop by an ATI clinic near you or schedule a complimentary screening at ATI Physical Therapy today!

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How Exercise Might “Clean” the Alzheimer’s Brain

How Exercise Might "Clean" the Alzheimer's Brain

For the 50 million individuals worldwide ailing from Alzheimer’s disease, the announcements by pharmaceutical giants earlier this year that they will end research on therapeutics were devastating. The news is even more devastating considering projections that 100 million more people will be diagnosed with Alzheimer’s disease across the globe by 2050, all potentially without a medical means to better their quality of life.

As it happens, though, the pursuit of a therapeutic has been given a lifeline. New research shows that physical exercise can “clean up” the hostile environments in the brains of Alzheimer’s mice, allowing new nerve cells in the hippocampus, the brain structure involved in memory and learning, to enable cognitive improvements, such as learning and memory. These findings imply that pharmacological agents that enrich the hippocampal environment to boost cell growth and survival might be effective to recuperate brain health and function in human Alzheimer’s disease patients.

The brain of an individual with Alzheimer’s disease is a harsh place filled with buildups of harmful nerve cell junk—amyloid plaques and neurofibrillary tangles—and dramatic loss of nerve cells and connections that occur with severe cognitive decline, such as memory loss. Targeting and disrupting this harmful junk, specifically amyloid plaques, to restore brain function has been the basis of many failed clinical trials. This futility has led to a re-evaluation of the amyloid hypothesis—the central dogma for Alzheimer’s disease pathology based on the toxic accumulation of amyloid plaques.

At the same time, there have been traces of evidence for exercise playing a preventative role in Alzheimer’s disease, but exactly how this occurs and how to take advantage of it therapeutically has remained elusive. Exercise has been shown to create biochemical changes that fertilize the brain’s environment to mend nerve cell health. Additionally, exercise induces restorative changes relevant to Alzheimer’s disease pathology with improved nerve cell growth and connectivity in the hippocampus, a process called adult hippocampal neurogenesis. For these reasons, the authors Choi et al. explored whether exercise-induced effects and hippocampal nerve cell growth could be utilized for therapeutic purposes in Alzheimer’s disease to restore brain function.

The researchers found that exercised animals from a mouse model of Alzheimer’s had greatly enhanced memory compared to sedentary ones due to improved adult hippocampal neurogenesis and a rise in amounts of a specific molecule that promotes brain cell growth called BDNF.  Importantly, they could recover brain function, specifically memory, in mice with Alzheimer’s disease but without exercise by increasing hippocampal cell growth and BDNF levels using a combination of genetic—injecting a virus—and pharmacological means. On the other hand, blocking hippocampal neurogenesis early in Alzheimer’s worsened nerve cell health later in stages, leading to degeneration of the hippocampus and, subsequently, memory function. This provides preclinical proof of concept that a combination of drugs that increase adult hippocampal neurogenesis and BDNF levels could be disease-modifying or prevent Alzheimer’s disease altogether.

With this work, things don’t look promising for the amyloid hypothesis—that Alzheimer’s disease is caused by the deposition of amyloid plaques. In this study, it was shown that eliminating amyloid plaques were not to necessary to ameliorate memory defects, which is consistent with evidence that plaques can also be found in the brains of healthy individuals. On the contrary, we may be looking at a new and improved fundamental theory for Alzheimer’s disease based on promoting a healthier brain environment and adult hippocampal neurogenesis.

However, this inspiring news should be taken with an important caution—mouse models of Alzheimer’s are notorious for failing to translate into humans such that treatments that have worked to remedy mice have failed for humans. Besides, even if these findings translate into humans, it may apply to a fraction of Alzheimer’s individuals with relevant genetic components to the mouse model utilized. Future studies will need to replicate these results in mouse models emulating the range of known Alzheimer’s disease genetic milieus and, more importantly, prove its medical relevance to human disease.

Before translating these findings into human patients, there remains significant research to establish that a medication or drug could mimic the effects of exercise—exercise mimetics—by “cleaning up” the brain with BDNF and stimulating neurogenesis to combat Alzheimer’s disease. Currently, the method for administering BDNF to animals in the lab—by direct injection into the brain—is not ideal for use in people, and a hippocampal neurogenesis stimulating compound remains elusive.

Future attempts to generate pharmacological means to imitate and heighten the benefits of exercise—exercise mimetics—to increase adult hippocampal neurogenesis in addition to BDNF may someday provide an effective means of improving cognition in people with Alzheimer’s disease. Moreover, increasing neurogenesis in the earliest stages of the disease may protect against neuronal cell death later in the disease, providing a potentially powerful disease-modifying treatment strategy.

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