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Showing posts with label NFL. Show all posts
Showing posts with label NFL. Show all posts
Friday, August 9, 2019
Routine hits playing football cause damage to the brain
Thursday, August 16, 2018
Free e-book: Concussions, CTE and Football
From the Introduction:
When You Watch Your Next Football Game...
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From high school to college to professional levels, football dominates American sports and exposes millions to head traumas on practically every play.
It is a paradox of wide proportions. From opening day in September to the Super Bowl in February, the National Football League (NFL) dominates American sports and wins television ratings far beyond any other program--sports or otherwise.
(Also available on Amazon and Kindle.)
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Increasingly, though, discussions of football (and other sports) include the medical terms concussion and chronic traumatic encephalopathy (CTE), a long-term degenerative and incurable brain disease. Although military personnel and others are vulnerable to the disease, the highest risk is among athletes involved in contact sports in which hits to the head are considered “part of the game.”
Ten years ago, few would have predicted that the movie “Concussion” starring Will Smith would be made. Fewer would have predicted that brain injuries would one day dominate the sports headlines. When former NFL star Junior Seau committed suicide in May 2012, the media focused almost entirely on whether the thousands of head blows he endured during his 19-year career as a middle linebacker were a contributing factor.
More than 3,000 former NFL players sued the league for allegedly misleading them about the risks of brain injury. The players and the league settled for more than $1 billion in damages. New policies and studies aimed at protecting the brains of athletes seem to be announced every week. But it’s not just professional athletes who are the focus of attention. No fewer than 40 states have passed laws requiring athletes in schools and recreational programs to schedule a doctor’s appointment when a concussion is suspected.
A progressive, degenerative brain disease, CTE can present itself in athletes and others with a history of repetitive brain trauma months, years, or even decades after injury. Memory loss, confusion, depression, aggression, impaired judgment or impulse control, and, eventually, progressive dementia may result.
With this increasing awareness about the dangers of concussion, parents face tough choices about which sports their children should be allowed to play. Some of the more
New rules have since been designed to lessen brain trauma; but with every new horror story that emerges on the sports pages, parents worry even more.
dangerous sports for the brain, such as football, soccer, ice hockey, and lacrosse, are also the most popular. Although everyone agrees that brain trauma may have lasting and debilitating effects, and science continues to make slow progress toward understanding the disease, we cannot yet entirely quantify those effects. As a result, parents and even medical professionals are left to search their hearts and scour Web sites for answers. But a decade’s worth of research has made one thing clear: We need to find better ways to protect the brains of athletes.
Difficult to Measure
Concussions suffer from a perception problem. On the surface, they might not seem to have a lasting, serious impact. (In fact, sports programs and commentators continue to celebrate the most impactful “hits,” using euphemisms such as “getting your bell rung.”) They are an invisible injury: There is no blood, there are no displaced bones, and the patient rarely complains. Even when an athlete is knocked unconscious and observers react with panic, the concern quickly fades. Ninety-nine percent of concussed athletes wake up in seconds or minutes and then seem fine. When symptoms persist beyond the day of injury, in the vast majority of cases they dissipate within a month. The injury seems as if it is gone forever, leaving no scars or overt indication that it ever happened.
Children at Risk
Most brain trauma in the industrialized world occurs in children playing sports. Since participation is voluntary, and the rules of recreational sports are malleable, it seems reasonable to make every effort to reform each individual sport....
Saturday, January 27, 2018
Hits, not concussions, cause CTE
It's Super Bowl week and America turns its eyes to the biggest event of the year. America loves its football. But will the game survive the concussion/CTE crisis affecting those who play the game?
New insights into the disease show head impact, not concussion, triggers CTE and pave way for early detection, prevention and treatment January 18, 2018 Boston University School of Medicine Researchers have identified evidence of early Chronic Traumatic Encephalopathy (CTE) brain pathology after head impact even in the absence of signs of concussion.
Early indicators of CTE pathology not only persisted long after injury but also spread through the brain, providing the best evidence to date that head impact, not concussion, causes CTE.
Researchers have identified evidence of early Chronic Traumatic Encephalopathy (CTE) brain pathology after head impact even in the absence of signs of concussion. Early indicators of CTE pathology not only persisted long after injury but also spread through the brain, providing the best evidence to date that head impact, not concussion, causes CTE.
The findings, published online in the journal Brain, are based on analysis of human brains from teenagers with recent head injury and mouse models that recreate sportsrelated head impact and militaryrelated blast exposure. The investigators also performed laboratory experiments and computer modeling. Study results shed light on the origins of CTE and relationship to traumatic brain injury (TBI), concussion and subconcussive head injury. CTE is a neurodegenerative disease characterized by abnormal accumulation of tau protein around small blood vessels in the brain. CTE causes brain cell death, cognitive deficits, and dementia. The brain pathology of CTE has been observed in brains of teenagers and adults with exposure to repeated head injury, both concussive and subconcussive episodes. However, the mechanisms that cause CTE and relationship to concussion, subconcussive injury and TBI remain poorly understood. In the first part of their study, the researchers examined four postmortem brains from teenage athletes who had sustained closedhead impact injuries 1, 2, 10 and 128 days prior to death. Neuropathological analysis of these brains showed a spectrum of posttraumatic pathology, including one case of earlystage CTE and two cases with abnormal accumulation of tau protein. Brains from four agematched athletes without recent head injury did not show the pathological changes observed in the headinjury group.
To investigate causal mechanisms underlying these changes, the researchers conducted laboratory experiments using mouse models of two different injury mechanisms repeat closedhead impact and blast exposure both linked to CTE. The investigators compared brain responses to the experimental injuries and relationship to CTE pathology over time. Based on pathological findings in human cases, the researchers hypothesized that early CTE may result from damaged blood vessels in the brain that become leaky, resulting in blood proteins spilling into brain tissue and triggering brain inflammation. The researchers utilized a brain scan called dynamic contrastenhanced magnetic resonance imaging (DCEMRI) to detect leaky blood vessels in the brains of mice subjected to head impact.
The investigators also found that head impact caused persistent changes in brain electrical functions, which may explain cognitive difficulties experienced by some people after these injuries. "The same brain pathology that we observed in teenagers after head injury was also present in headinjured mice. We were surprised that the brain pathology was unrelated to signs of concussion, including altered arousal and impaired balance, among others. Our findings provide strong causal evidence linking head impact to TBI and early CTE, independent of concussion," explained corresponding author Lee E. Goldstein, MD, PhD, an associate professor at Boston University School of Medicine and College of Engineering. "The results may explain why approximately 20 percent of athletes with CTE never suffered a diagnosed concussion."
Source: ScienceDaily, Boston University
New insights into the disease show head impact, not concussion, triggers CTE and pave way for early detection, prevention and treatment January 18, 2018 Boston University School of Medicine Researchers have identified evidence of early Chronic Traumatic Encephalopathy (CTE) brain pathology after head impact even in the absence of signs of concussion.
Early indicators of CTE pathology not only persisted long after injury but also spread through the brain, providing the best evidence to date that head impact, not concussion, causes CTE.
Researchers have identified evidence of early Chronic Traumatic Encephalopathy (CTE) brain pathology after head impact even in the absence of signs of concussion. Early indicators of CTE pathology not only persisted long after injury but also spread through the brain, providing the best evidence to date that head impact, not concussion, causes CTE.
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| Learn about the brain in simple language. |
The findings, published online in the journal Brain, are based on analysis of human brains from teenagers with recent head injury and mouse models that recreate sportsrelated head impact and militaryrelated blast exposure. The investigators also performed laboratory experiments and computer modeling. Study results shed light on the origins of CTE and relationship to traumatic brain injury (TBI), concussion and subconcussive head injury. CTE is a neurodegenerative disease characterized by abnormal accumulation of tau protein around small blood vessels in the brain. CTE causes brain cell death, cognitive deficits, and dementia. The brain pathology of CTE has been observed in brains of teenagers and adults with exposure to repeated head injury, both concussive and subconcussive episodes. However, the mechanisms that cause CTE and relationship to concussion, subconcussive injury and TBI remain poorly understood. In the first part of their study, the researchers examined four postmortem brains from teenage athletes who had sustained closedhead impact injuries 1, 2, 10 and 128 days prior to death. Neuropathological analysis of these brains showed a spectrum of posttraumatic pathology, including one case of earlystage CTE and two cases with abnormal accumulation of tau protein. Brains from four agematched athletes without recent head injury did not show the pathological changes observed in the headinjury group.
To investigate causal mechanisms underlying these changes, the researchers conducted laboratory experiments using mouse models of two different injury mechanisms repeat closedhead impact and blast exposure both linked to CTE. The investigators compared brain responses to the experimental injuries and relationship to CTE pathology over time. Based on pathological findings in human cases, the researchers hypothesized that early CTE may result from damaged blood vessels in the brain that become leaky, resulting in blood proteins spilling into brain tissue and triggering brain inflammation. The researchers utilized a brain scan called dynamic contrastenhanced magnetic resonance imaging (DCEMRI) to detect leaky blood vessels in the brains of mice subjected to head impact.
The investigators also found that head impact caused persistent changes in brain electrical functions, which may explain cognitive difficulties experienced by some people after these injuries. "The same brain pathology that we observed in teenagers after head injury was also present in headinjured mice. We were surprised that the brain pathology was unrelated to signs of concussion, including altered arousal and impaired balance, among others. Our findings provide strong causal evidence linking head impact to TBI and early CTE, independent of concussion," explained corresponding author Lee E. Goldstein, MD, PhD, an associate professor at Boston University School of Medicine and College of Engineering. "The results may explain why approximately 20 percent of athletes with CTE never suffered a diagnosed concussion."
Source: ScienceDaily, Boston University
Wednesday, December 6, 2017
Steeler's football injury: Protecting the miraculous, fragile spinal cord
Source: USA Today
As Ryan Shazier continues to undergo tests at the University of Cincinnati Medical Center for a spine injury, he tweeted a thank-you Tuesday evening.
Shazier was injured during the Pittsburgh Steelers' win over the Cincinnati Bengals onMonday Night Football. He was taken by ambulance to the hospital after being removed from the field on a backboard.
"Thank you for the prayers. Your support is uplifting to me and my family. #SHALIEVE"
Earlier Tuesday, team general manager Kevin Colbert said Shazier is not expected to need surgery. Doctors released a statement that said he will remain hospitalized for more tests and evaluations during the next 24-48 hours.
Shazier underwent a CT scan and MRI after being injured in the first quarter of the Steelers' 23-20 win.
After he tackled receiver Josh Malone with the crown of his helmet, he slumped to the turf and his body went limp. He later grabbed his middle back and it appeared he was having trouble moving his legs.
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| Learn about the brain, the spinal cord and the central nervous system in easy-to-read form. |
Source: National Institute of Neurological Disorders and Stroke:
How does the spinal cord work? To understand what can happen as the result of a spinal cord injury, it is important to understand the anatomy of the spinal cord and its normal functions. The spinal cord is a tight bundle of neural cells (neurons and glia) and nerve pathways (axons) that extend from the base of the brain to the lower back. It is the primary information highway that receives sensory information from the skin, joints, internal organs, and muscles of the trunk, arms, and legs, which is then relayed upward to the brain. It also carries messages downward from the brain to other body systems.
Millions of nerve cells situated in the spinal cord itself also coordinate complex patterns of movements such as rhythmic breathing and walking. Together, the spinal cord and brain make up the central nervous system (CNS), which controls most functions of the body. The spinal cord is made up of neurons, glia, and blood vessels. The neurons and their dendrites (branching projections that receive input from axons of other neurons) reside in an H-shaped or butterfly-shaped region called gray matter. The gray matter of the cord contains lower motor neurons, which branch out from the cord to muscles, internal organs, and tissue in other parts of the body and transmit information commands to start and stop muscle movement that is under voluntary control.
Upper motor neurons are located in the brain and send their long processes (axons) to the spinal cord neurons. Other types of nerve cells found in dense clumps of cells that sit just outside the spinal cord (called sensory ganglia) relay information such as temperature, touch, pain, vibration, and joint position back to the brain. The axons carry signals up and down the spinal cord and to the rest of the body. Thousands of axons are bundled into pairs of spinal nerves that link the spinal cord to the muscles and the rest of the body. The function of these nerves reflects their location along the spinal cord. 4 • Cervical spinal nerves (C1 to C8) emerge from the spinal cord in the neck and control signals to the back of the head, the neck and shoulders, the arms and hands, and the diaphragm. • Thoracic spinal nerves (T1 to T12) emerge from the spinal cord in the upper mid-back and control signals to the chest muscles, some muscles of the back, and many organ systems, including parts of the abdomen.
Lumbar spinal nerves (L1 to L5) emerge from the spinal cord in the low back and control signals to the lower parts of the abdomen and the back, the buttocks, some parts of the external genital organs, and parts of the leg. Between the vertebrae of the spinal column are discs that act as passages through which the spinal nerves travel. These places are particularly vulnerable to injury
Thursday, September 21, 2017
Aaron Hernandez' CTE diagnosis 'devastating' news for NFL
From Yahoo News (Sept. 21, 2017):
"Based on his violent outbursts, mood swings and self-medicating ways, it comes as little surprise that Aaron Hernandez suffered from chronic traumatic encephalopathy (CTE), as his lawyer alleges in a new lawsuit against the NFL and the New England Patriots.
The degenerative brain disease has been most commonly found in football players, soldiers and others who have suffered from repeated concussions.
“Aaron had Stage III CTE usually seen in players with a median age of death of 67 years,” reads a lawsuit attorney, Jose Baez, filed in the name of Hernandez’s daughter, Avielle.
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| Learn more about concussions, CTE, and football. |
It may explain, yet hardly excuse, Hernandez of murdering Odin Lloyd in 2013 or being charged for the 2012 slaying of Daniel de Abreu and Safiro Furtado. He beat the double murder because while there was no disputing he was in the car the night of the drive-by shooting, prosecutors couldn’t conclusively prove he was the triggerman. It may also provide insight into his prison suicide last spring while serving a life sentence for the Lloyd killing.
Based on his age, however, a CTE diagnosis this significant comes as not just a surprise, but a chilling moment for a sport that is trying everything to both make the game safer and convince young athletes, and their parents, that it is worth playing.
Sixty-seven years old? Advanced stages? That is the opinion of researchers at Boston University, who have been the leaders on CTE research.
Hernandez played just three seasons in the NFL, 44 games total for the Patriots, before being arrested at the age of 23 for the Lloyd murder. He was 27 when he took his life...."
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