PROTECTING OUR CHILDREN FROM DANGER

Are we keeping our children and youth safe from the wrong dangers?

Moms take their children in the car, in a state-of-the-art car seat or seat belt to go and play football, because car accidents have been a leading cause of child injury in the past.

From the statistics, Concussion risk and taking the head our of football and other Sports, Recreation and Exercise has not been properly controlled and supervised.

An estimated 300,000 sports-related concussions occur annually in the United States. Between 2001 and 2009, emergency room visits for brain injuries among children and adolescents increased 62% (up from 153,375 to 248,314). (CDC) Most likely the increase are from recreational activities with bicycling, football, playground activities, basketball and soccer most likely to lead to injuries. (CDC)

Chronic Traumatic Encephalopathy (CTE) and the dementia that can follow from Sports Concussion are the only fully preventable causes of dementia (deterioration of the brain’s intelligence and other vital functions), said Robert Cantu, MD.

INCREASE IN CONCUSSIONS AND CONCUSSION AWARENESS

•Between 2001 and 2009, emergency room visits for brain injuries among children and adolescents increased 62% (up from 153,375 to 248,314). (CDC)
•Most likely causes are from recreational activities with bicycling, football, playground activities, basketball and soccer most likely to lead to injuries. (CDC)
•More than 500,000 concussions in the United States are sustained by the 4.4 million children who play tackle football. (Nat. Center for Sport Injury Research)
•Among males 10-19 football is the most common cause of concussion; among females 10-19 the most common causes are soccer, basketball and bicycling. (CDC)
•CDC believes the increases in emergency room visits are a result of: ◦Increased participation in sports
◦Increased incidence of concussion
◦Increased awareness by parents, coaches and the public at large about the need for medical attention after injury

CONCUSSION IN ADOLESCENTS IS A HEALTH CONCERN
•At least 50 high school or younger football players in more than 20 states since 1997 have been killed or have sustained serious head injuries on the field (NY Times 9/17/2007)
•Nearly 15% of sports related injuries in high school athletes are from concussion (Meehan et al, Am J Sports Med 2011 Oct 3)
•Some 136,000 high school students experience a concussion during an academic year. (Mayo Clinic)
•Concussion can occur even without a blow to the head (Mayo) and 90% of concussions are not associated with loss of consciousness
•All concussions should be considered serious, although most cause symptoms that last a short time. However, repeated concussions take longer to resolve and may risk permanent neurological damage (Mayo)
[Facts About Sports Concussion from the American Headache Society, SCOTTSDALE, AZ November 10, 2011]

“We certainly make constant (mis)calculations in our adult lives, we seem all the more determined yet befuddled when it comes to the safety of our children.”

The 5 most likely causes of injury to children up to age 18 are: car accidents, homicide (usually at the hands of someone they know), child abuse, suicide or drowning (CDC).

The 5 dangers that parents are most worried about (Mayo Clinic) are kidnapping, school snipers, terrorists, dangerous strangers and drugs.

“Parents are just bad at risk assessment,” said Christie Barnes, a mother of four and the author of “The Paranoid Parents Guide.” “We are constantly overestimating rare dangers while underestimating common ones.”

“You read the news about that poor football player, right? The University of Pennsylvania lineman who killed himself? And the autopsy, which showed that his head had been rattled by all those blows over the years? And the fact that the damage may have caused depression and lack of impulse control, which may have resulted in his suicide?”

“Football accounts for 22 percent of all concussions among 8 to 19 year-olds; 27% of football players ages 12 through 17 have had a least one concussion.”

“That will not be news to any mother, but what will be news is last week’s link between teenage football and chronic traumatic encephalopathy (CTE). Owen Thomas, the 21 Penn student who killed himself in April, was found to have CTE by Boston University researchers.

“A kid growing up has to go through 7 different changes of car seat by law in some states,” said Dr. Daniel Perl, a professor of pathology at Uniformed Services University of the Health Sciences in Bethesda, Md., the medical school for the United States military, “and what that prevents in terms of injuries or deaths are probably a couple of handfuls. Yet we have over four million kids playing football. Moms will take their 7-year-olds in the car, in a state-of-the-art car seat, to go and play football.” [Keeping Kids Safe From the Wrong Dangers, by Lisa Belkin, September 18, 2010, New York Times]

When the Coach of youth football in the South End, heard about a game in central Massachusetts where five players sustained concussions, he was very disturbed.

The adults in charge “did not stop the lopsided game even when the losing team could not field the required number of healthy players. There was no reason for that game to keep going.”

After Pop Warner game, “Coaches and parents said they were aghast at the number of injuries in the September game, and the failure of adults to intervene on the children’s behalf during the 52-0 mismatch.”

“Josh Pruce, a spokesman for the national Pop Warner group, said that he had never heard of a game where so many players suffered concussions, and that officials should have ended the game as soon as Tantasqua’s injuries began to mount.

“Parents say the issue is not that youth football lacks rules and safety precautions; the problem is when those rules and precautions are ignored.” [Concussions bring more scrutiny in youth football by Peter Schworm, Oct. 23, 2012, boston.com]

Moms, dads and guardians, at the first football team organizational meeting or practice, ask the Coach about his/her Concussion precautions? Question helmet and equipment safety, potential size, age and strength mismatches that might occur in practices and games, how the head is taken our of the game during blocking and tackeling drills and during the games. If the Coach blows-off the questions, are not concerned, act as if those are ignorant questions and/or does not have resonable answers, seek another team, Coach and/or Sport.

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Abstract

“Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disease that is a long-term consequence of single or repetitive closed head injuries for which there is no treatment and no definitive pre-mortem diagnosis. It has been closely tied to athletes who participate in contact sports like boxing, American football, soccer, professional wrestling and hockey. Risk factors include head trauma, presence of ApoE3 or ApoE4 allele, military service, and old age. It is histologically identified by the presence of tau-immunoreactive NFTs and NTs with some cases having a TDP-43 proteinopathy or beta-amyloid plaques.

“It has an insidious clinical presentation that begins with cognitive and emotional disturbances and can progress to Parkinsonian symptoms. The exact mechanism for CTE has not been precisely defined however, research suggest it is due to an ongoing metabolic and immunologic cascade called immunoexcitiotoxicity.

“Prevention and education are currently the most compelling way to combat CTE and will be an emphasis of both physicians and athletes. Further research is needed to aid in pre-mortem diagnosis, therapies, and support for individuals and their families living with CTE.

“The course of symptom progression seems to follow a somewhat continuous path beginning with cognitive and emotional decline leading to eventual motor deterioration [5].

“Initially, patients begin to have poor concentration, attention, and memory along with disorientation, dizziness, and headaches. They typically progress to experience irritability, outbursts of violent or aggressive behavior, confusion, and speech abnormalities. During this stage of the disease, there is a high frequency of suicide, drug overdose, and mood disorders, mainly major depressive disorder [5].

“A study by Omalu and colleagues describes a similar clinical profile with a latent asymptomatic period between play and symptom onset. He reports worsening of cognitive and social functioning leading to poor money management, bankruptcy, social phobias, paranoid ideation, insomnia, poor relationships, divorce, emotional/physical abuse, and substance abuse [18]. Family and friends of the affected individuals reported many of these symptoms to researchers through standard forensic interviews [18].

As the disease progresses in severity, there is a greater loss of motor functioning. Some patients may develop Parkinsonian symptoms of tremors, masked facieses, wide propulsive gait, poor speech, ocular abnormalities, vertigo, bradykinesia, deafness, and a small group developing dementia. Currently, the number of cases with confirmed dementia remains small.
“As more postmortem exams are done in the at risk group, it is expected more cases will be diagnosed. Some individuals with CTE have committed suicide, overdosed on drugs, or died from accidents preventing progression of the disease [5, 20].

Clinicopathologic Correlations

“The typical symptoms of CTE can be directly connected to the specific areas of the brain that are injured during the progression of disease. Based on these symptoms it is clear that there is damage to the hippocampal-septo-hypothalamic-mesencephalic circuitry (Papez circuit) also known as the emotional or visceral brain [5]. Damage to these areas correlate to the behavioral symptoms of emotional liability, aggression, and violence. Damage to the hippocampus, enteorhinal cortex, and medial thalamus conceivably causes the commonly reported complaint of memory disturbance. Destruction to the frontal cortex and white matter may result in the dysexecutive symptoms found throughout the many cases of CTE. Motor abnormalities may be due to degeneration of the substantia nigra and pars compacta along with symptoms of dysarthria, dysphagia, and ocular malfunction due to brainstem nuclei injury like the hypoglossal and oculomotor nuclei (see Table 4) [5].

[Chronic Traumatic Encephalopathy: A Review. Michael Saulle and Brian D. Greenwald, Rehabilitation Research and Practice, Volume 2012 (2012), Article ID 816069]
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Abstract

“Since the 1920s, it has been known that the repetitive brain trauma associated with boxing may produce a progressive neurological deterioration, originally termed “dementia pugilistica” and more recently, chronic traumatic encephalopathy (CTE).

We review the 47 cases of neuropathologically verified CTE recorded in the literature and document the detailed findings of CTE in 3 professional athletes: one football player and 2 boxers. Clinically, CTE is associated with memory disturbances, behavioral and personality changes, Parkinsonism, and speech and gait abnormalities. Neuropathologically, CTE is characterized by atrophy of the cerebral hemispheres, medial temporal lobe, thalamus, mammillary bodies, and brainstem, with ventricular dilatation and a fenestrated cavum septum pellucidum.

“Microscopically, there are extensive tau-immunoreactive neurofibrillary tangles, astrocytic tangles, and spindle-shaped and threadlike neurites throughout the brain. The neurofibrillary degeneration of CTE is distinguished from other tauopathies by preferential involvement of the superficial cortical layers, irregular, patchy distribution in the frontal and temporal cortices, propensity for sulcal depths, prominent perivascular, periventricular and subpial distribution, and marked accumulation of tau-immunoreactive astrocytes. Deposition of beta amyloid, most commonly as diffuse plaques, occurs in fewer than half the cases. CTE is a neuropathologically distinct, slowly progressive tauopathy with a clear environmental etiology.

Clinical and Demographic Features of CTE

“The concept of CTE was first introduced by Martland in 1928 who introduced the term ‘punch-drunk’ to a symptom complex that appeared to be the result of repeated sublethal blows to the head (26). This syndrome, long recognized in professional boxers, was termed “dementia pugilistica” by Millspaugh (27) and “the psychopathic deterioration of pugilists” by Courville (28). The symptoms of CTE are insidious, first manifest by deteriorations in attention, concentration, and memory, as well as disorientation and confusion, and occasionally accompanied by dizziness and headaches. With progressive deterioration, additional symptoms, such as lack of insight, poor judgment, and overt dementia, become manifest. Severe cases are accompanied by a progressive slowing of muscular movements, a staggered, propulsive gait, masked facies, impeded speech, tremors, vertigo, and deafness (27). Corsellis, Bruton, and Freeman-Browne described 3 stages of clinical deterioration as follows: The first stage is characterized by affective disturbances and psychotic symptoms. Social instability, erratic behavior, memory loss, and initial symptoms of Parkinson disease appear during the second stage.

“The third stage consists of general cognitive dysfunction progressing to dementia and is often accompanied by full-blown Parkinsonism, as well as speech and gait abnormalities. Other symptoms include dysarthria, dysphagia, and ocular abnormalities, such as ptosis (29). The severity of the disorder appears to correlate with the length of time engaged in the sport and the number of traumatic injuries, although whether a single traumatic brain injury can trigger the onset of CTE remains a matter of speculation.

“Of the 51 neuropathologically confirmed cases of CTE, 46 (90%) occurred in athletes. The athletes included 39 boxers (85%) who fought as amateurs and as professionals for varying lengths of time (range: 4 to 25 years; mean: 14.4 years), 5 football players (11%), whose playing time ranged between 14 and 23 years (M = 18.4 years, SD = 3.9); 1 professional wrestler, and 1 soccer player. The athletes began their respective sports at young ages, i.e. between 11 and 19 years (M = 15.4 years, SD = 2.2) (Tables 1, ,2).2). The first symptoms of CTE were noticed at ages ranging from 25 to 76 years (M = 42.8 years, SD = 12.7).

“One third were symptomatic at the time of their retirement from the sport and half were symptomatic within 4 years of stopping play. Common presenting symptoms included memory loss, irritability, outbursts of aggressive or violent behavior, confusion, speech abnormalities, cognitive decline, gait abnormalities, unsteadiness, headaches, slurred speech and Parkinsonism. In 14 cases (30%) there was a prominent mood disturbance, usually depression (28%); 1 boxer was described as having a “euphoric dementia” (31); another boxer was described as manic-depressive (35); and a football player was considered “bipolar” (40). In most of the reported cases, the disease progressed slowly over several decades (range: 2–46 years; M = 18.6 years, SD = 12.6) with increasing abnormalities in behavior and personality, memory loss, cognitive decline, and visuospatial difficulties. Movement abnormalities were eventually found in 42% subjects, consisting of Parkinsonism, staggered, slowed or shuffled gait, slowed, slurred or dysarthric speech, ataxia, ocular abnormalities and dysphagia. As Critchley noted in 1957, “Once established it not only does not permit reversibility, but ordinarily advances steadily, even though the boxer has retired from the ring”(42).

[Chronic Traumatic Encephalopathy in Athletes: Progressive Tauopathy following Repetitive Head Injury, Ann C. McKee, MD,1,2,3,4 Robert C. Cantu, MD,3,5,6,7 Christopher J. Nowinski, AB,3,5 E. Tessa Hedley-Whyte, MD,8 Brandon E. Gavett, PhD,1 Andrew E. Budson, MD,1,4 Veronica E. Santini, MD,1 Hyo-Soon Lee, MD,1 Caroline A. Kubilus,1,3 and Robert A. Stern, PhD1,3 J Neuropathol Exp Neurol. 2009 July; 68(7): 709–735. ]

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Abstract

“Chronic traumatic encephalopathy (CTE) is a form of neurodegeneration that results from repetitive brain trauma. Not surprisingly, CTE has been linked to participation in contact sports such as boxing, hockey and American football. In American football getting “dinged” equates to moments of dizziness, confusion, or grogginess that can follow a blow to the head. There are approximately 100,000 to 300,000 concussive episodes occurring in the game of American football alone each year.

“It is believed that repetitive brain trauma, with or possibly without symptomatic concussion, sets off a cascade of events that result in neurodegenerative changes highlighted by accumulations of hyperphosphorylated tau and neuronal TAR DNA-binding protein-43 (TDP-43). Symptoms of CTE may begin years or decades later and include a progressive decline of memory, as well as depression, poor impulse control, suicidal behavior, and, eventually, dementia similar to Alzheimer’s disease. In some individuals, CTE is also associated with motor neuron disease similar to amyotrophic lateral sclerosis. Given the millions of athletes participating in contact sports that involve repetitive brain trauma, CTE represents an important public health issue.

“In this review, we discuss recent advances in understanding the etiology of CTE. It is now known that those instances of mild concussion or “dings” that we may have previously not noticed could very well be causing progressive neurodegenerative damage to a player’s brain. In the future, focused and intensive study of the risk factors could potentially uncover methods to prevent and treat this disease.

Conclusion

“CTE is a neuropathologically distinct neurodegenerative disease that is believed to result from repetitive brain trauma as frequently occurs in popular contact sports. Early symptoms of CTE include a decline of memory and cognitive functioning, depression, poor impulse control and in many cases suicide. Disease progression is slow and eventually leads to dementia. In some individuals CTE may also lead to a motor neuron disease similar to ALS. What was once believed to occur only in boxers is now openly discussed as a potential consequence of repetitive brain trauma seen in multiple different sports and at all levels of play. Although we now know that repetitive brain trauma sets off a cascade of molecular events that results in neurodegeneration marked by a unique taupathy and TDP-43 proteinopathy, we do not know the underlying mechanism of the disease. How can CBT be detected and diagnosed accurately during life?

“ How can CBT be prevented and treated? By addressing these important questions, CBT can move from a disease only diagnosed postmortem to one that can be identified, treated, and cured in life. In addition, new research will provide policy makers with scientific data to make appropriate guidelines regarding the treatment of brain trauma in athletes and military personnel. Given the millions of athletes both young and old participating in contact sports that involve repetitive brain trauma, CTE remains an important and expanding health issue with unmet medical need.

[Chronic traumatic encephalopathy: the dangers of getting “dinged”, Shaheen E Lakhan, Global Neuroscience Initiative Foundation, Los Angeles, CA, USA and Annette Kirchgessner School of Health and Medical Sciences, Seton Hall University, South Orange, NJ, USA

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