Dementia pugilistica

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Dementia pugilistica ( lat. Dementia "madness", pugilistica "pugilistic") and chronic traumatic encephalopathy (CTE), Boxer encephalopathy , fist combative Parkinson's disease , Boxer Syndrome or Punch-Drunk Syndrome is a neural dysfunction that after frequent beatings or Bumps to the head occurs. In the meantime, the sport-neutral designation CTE has become the most common. The term punch drunk was previously used broadly to refer to second rate fighters used for training purposes.

Course and diagnosis

Left a normal brain and right a brain with CTE

CTE is an independent neurological disease (slowly progressing tauopathy ) with a clear cause based on external influences (head injuries). As far as we know today, every neuropathologically confirmed CTE case is associated with previous repeated blows or bumps to the head. The neural degeneration is probably the result of small, traumatic bleeding. CTE usually occurs years after the end of a sports career with a progressive course. In 34 American football players whose brain was histologically examined after their death, the degree of CTE correlated with the length of time they played sports, the time after completing their sports careers and the age of death.

CTE cannot be diagnosed clinically so far, but only post mortem through histological analysis of the brain. Clinically, CTE is associated with increasing memory loss, behavior and personality changes, parkinsonism, speech disorders, slower gait as well as depression , the risk of suicide , aggressiveness and possible dementia . Some patients also have motor neuron diseases that are clinically similar to amyotrophic lateral sclerosis .

Neuropathologically, there is atrophy of the cerebral halves, the medial temporal lobe , the thalamus , the mamillary bodies and the brain stem , accompanied by ventricular enlargements . Microscopically, abnormal deposits of hyperphosphorylated tau proteins can be found in the form of neurofibrillar aggregates, aggregates in glial astrocytes and neuropil threads throughout the brain. These gradually lead to the death of brain cells. The neurofibrillary degeneration in CTE differs from other tauopathies in that the superficial layers of the cerebral cortex are predominantly affected and a patchy distribution occurs in the frontal and temporal cerebral cortex. The noticeable accumulation of tau proteins in the astrocytes is also characteristic. Scientists assume that repeated traumatic brain injuries that are associated with a concussion or remain subliminal without symptoms of a concussion are responsible for the neurodegenerative changes that result in the accumulation of hyperphosphorylated tau proteins and TDP- 43 proteins express.

After specific pathological criteria for diagnosing CTE have been established, the disease is divided into four grades. This is based on post-mortem examinations, which were related to behavioral problems identified before death.

  • Stage I: headache, attention and concentration deficits
  • Stage II: additional symptoms such as depression, emotional outbursts, impaired short-term memory
  • Level III: Cognitive impairments, problems in planning and organizing everyday activities, multitasking problems, deficiencies in judgment
  • Stage IV: pronounced dementia with severe memory and cognitive disorders that make it impossible to cope with everyday life

CTE is similar to Parkinson's disease in terms of the decreased ability to coordinate, which can lead to speech problems, unsteady gait and unusual behavior .

cases

At least 69 cases of CTE have been reported in the literature between 2000 and 2015. The CTE syndrome , which is called Traumatic Encephalopathy Syndrome (TES) according to clinical criteria and in which CTE was finally confirmed posthumously in autopsies, is very common in boxers or American football players who have been active for many years , but also in people who are addicted to alcohol often suffer falls and are unable to support themselves due to their reduced ability to react. Naturally, the number of frequent head butts and thus the CTE risk in the collision sports of boxing and American football is particularly high. Here the players can experience more than 1000 shocks per year without these already triggering concussions. Repeated internal head injuries with serious long-term consequences have also been observed in wrestling and rugby as well as in ice hockey , handball, lacrosse, skiing, karate , judo , wrestling , horse riding, parachuting and football .

American football

Neuropathologist Bennet Omalu published three neurohistological case studies of CTE in ex-American professional football players in 2005, 2006 and 2010. These cases involved NFL players Mike Webster (1952-2002), Terry Long (1959-2005) and Andre Waters (1962-2006). The story of some of these players is taken up in the 2016 movie, Shattering Truth .

Other examples of well-known NFL players who died from or with CTE syndrome are Tom McHale (1963-2008), Justin Strzelczyk (1968-2004), Dave Duerson (1960-2011) and Chris Henry (1983-2009) , the first known case of an active football player with the disease.

In January 2016, the former running back Lawrence Phillips (1975-2016) killed himself in his prison cell. He had become a criminal offender through a number of acts of violence. His family donated Phillips' brain to Boston University's CTE Center for post-mortem examinations for CTE. Likewise, former tight end Aaron Hernandez committed suicide in 2017 at the age of 27 after being convicted of murder in 2015. He suffered from CTE at an advanced stage, which researchers normally only found in sick players who were on average 40 years older than Hernandez.

In Germany, on April 8, 2017, the Süddeutsche Zeitung reported for the first time on the connection between American football and CTE in Europe. The first quarterback of the German national team, the Ansbacher Erich Grau, has been showing symptoms typical for CTE for almost twenty years.

baseball

The baseball player Ryan Freel (1976-2012) was determined to have CTE level II after his suicide during a brain autopsy. Freel was the first major league baseball player to receive such a diagnosis. Nine or ten concussions have been reported from his career.

Boxing

Well-known boxing victims who were believed to have CTE are Jack Dempsey (1895–1983), Joe Louis (1914–1981), Beau Jack (1921–2000), Jerry Quarry (1945–1999) and Sugar Ray Robinson (1921 –1989) and Bobby Chacon . When Paul Pender (1930-2003) CTE was identified in a neuropathological examination of his brain posthumously. Muhammad Ali, on the other hand, probably suffered from a pugilistic form of Parkinson's disease, as did Freddy Roach . A connection between her illnesses and boxing has not been proven, but it is quite likely.

Bull riding

The first case of CTE in professional bull riding was published in 2017. It concerned Canadian rider Ty Pozzobon who died by suicide at the age of 25 and who had suffered 15 head injuries within 10 years, including the first diagnosed concussion at the age of 16.

ice Hockey

Five cases of CTE have been diagnosed in professional ice hockey so far, namely in the former NHL players Reg Fleming (1936-2009), Bob Probert (1965-2010), Rick Martin (1951-2011), Derek Boogaard (1982-2011) and Steve Montador (1979-2015). Montador, whose family has sued the NHL for reimbursement, suffered at least three concussions in six months in 2003, at least four in nine months in 2010, and at least four in three months in 2012.

Soccer

In football, chronic traumatic encephalopathy has been diagnosed in two well-known professional players, namely Jeff Astle (1942–2002) and Hilderaldo Bellini (1930–2014). Both had developed Level IV CTE. A third soccer player, who had played as a striker in the English Premier League for 16 years and died of dementia at the age of 70, had the anatomical and histopathological features typical of CTE, such as prominent atrophies in the entorhinal cortex, hippocampus and mammary bodies as well as dew-positive neurofibrillary tangles in the neocortex, described in a scientific publication. The semi-professional soccer player Patrick Grange (1982–2012) was also posthumously diagnosed with CTE level II.

Mixed martial arts

The first MMA fighter to be posthumously diagnosed with CTE is Jordan Parsons (1990-2016), who died in a car accident in May 2016 at the age of 25.

rugby

A very serious case of CTE (Level IV) was found in the 77-year-old former Australian rugby player Barry 'Tizza' Taylor (1936-2013), who played rugby competitively for 19 years, 235 games for the professional Manly Rugby Union team denied. Taylor died of profound dementia and had developed increasing cognitive problems ten years before his death.

Wrestling

In professional wrestling, the cases of Chris Benoit (1967-2007) and Andrew Test Martin (1975-2009) are known. Martin died of a drug overdose at the age of 33.

The WWE -Wrestler Daniel Bryan was for medical reasons, forced in February 2016 to withdraw from active sports because brain problems were detected at a check-up and because he had developed after concussions seizures. Bryan had suffered at least ten concussions in his 16-year career, including three in the first five months alone. Bryan said: “The truth is, I've been wrestling since I was 18 years old, and within the first five months of my wrestling career, I'd already had three concussions. And for years after that, I would get a concussion here and there, here or there, and then it gets to the point when you've been wrestling for 16 years, that adds up to a lot of concussions. It gets to a point where they tell you that you can't wrestle anymore. " After he stepped down, Bryan urged young athletes to report concussions and rest long enough. "You have a responsibility to yourself, your families and your friends," he appealed.

American WWE wrestler Balls Mahoney died in April 2016 at the age of 44. In October 2016, after an autopsy of his brain by forensic pathologist Bennet Omalu, it was announced that he suffered from CTE.

The American WWE wrestler Chyna (real name: Joan Marie Laurer), often seen as the pioneer of modern women's wrestling, died on April 20, 2016 as a result of a mixture of psychotropic drugs, painkillers and alcohol. According to her manager, her brain was made available to CTE scientists.

History

One of the earliest histopathological investigations into anatomical brain changes dates back to 1954. The boxer described in it, who died of a cerebral haemorrhage at the age of 51, had a blurred speech, forgetfulness and irritability. In the last year of his life he suffered from Parkinson's and dementia. His brain had senile plaque buildup with neurofibrils trapped in the cortex and decreased cerebellar volume.

For many years, signs and symptoms of CTE in ex-boxers were reported in a number of isolated individual cases. For a long time, the explanation of this syndrome was based solely on anecdotal evidence as well as analogies and guesswork. In 1973 a publication "Das Nachspiel des Boxens" (The aftermath of boxing) appeared, in which the findings of 15 neuropathologically examined former boxers were compiled. This resulted for the first time in grading CTE into several degrees of severity.

In a review article from 2009, 51 cases of CTE that had previously been confirmed neuropathologically were analyzed . Of these 51 cases, 46 (90%) occurred in professional athletes. Among the athletes affected were 39 boxers (85%), five American football players (11%), and a professional wrestler and a soccer player. On average, boxers had been active for 14.4 years and football players for 18.4 years.

A very large cohort comes from 2015 and includes 153 case studies, all neuropathologically reported cases of CTE between 1954 and 2013. The 153 cases included 69 (45.1%) former boxers, 63 (41.2%) former amateur and professional football players, 5 (3.3%) former ice hockey players, 6 (3.9 %) former war veterans and 3 (2.0%) former professional wrestlers. The meta-study was funded by the NFL and the Pittsburgh Steelers and directed by Joseph Maroon , who is a consultant and neurosurgeon for the Pittsburgh Steelers and medical director for World Wrestling Entertainment . The study identified mild traumatic brain injuries as the sole risk factor for CTE. No relationship was established between CTE and age at death. Suicide and premorbid dementia were also not strongly associated with CTE. The authors concluded that the incidence of CTE remains unclear due to the lack of longitudinal studies ("We conclude that the incidence of CTE remains unknown due to the lack of large, longitudinal studies.") Whether multiple head butts with harrowing and sub-harrowing effects the cause of the CTE remains speculative. But the increasing number of scientific reports is raising concerns about the cognitive consequences of repetitive exercise-related concussions.

Also from 2015 comes a joint neurohistological study by the Mayo Clinic in Florida and Boston University, which was carried out on 1,721 brains of deceased men with neurodegenerative disorders. Cortical tau proteins served as markers for diagnosing CTE. Twenty-one of 66 previous athletes who had amateur-level contact sports as teenagers in American high schools had tauopathy . In contrast, none of 198 subjects who had had no contact sports experience were found to have tauopathy. However, 33 of these had experienced traumatic brain injuries in individual cases, from falls, motorcycle accidents or domestic violence. Since the neurohistopathological symptoms of CTE were only discovered in those individuals who had documented participation in contact sports, it was concluded that this contact represented the greatest risk of developing CTE.

Against the background of the ongoing debate about prevalence and causal relationship, the '4. International Consensus Conference on Concussion in Sport ', which was co-organized by FIFA and hosted in Zurich, reached a consensus as follows:

"Clinicians need to be mindful of the potential for long-term problems in the management of all athletes. However, it was agreed that chronic traumatic encephalopathy (CTE) represents a distinct tauopathy with an unknown incidence in athletic populations. It was further agreed that a cause and effect relationship has not as yet been demonstrated between CTE and concussions or exposure to contact sports. At present, the interpretation of causation in the modern CTE case studies should proceed cautiously. It was also recognized that it is important to address the fears of parents / athletes from media pressure related to the possibility of CTE. "

In the United States of America, athletes are increasingly making their brains available for posthumous CTE analysis. This concerns, for example, the 192-time ex-national soccer player and world champion Brandi Chastain (* 1968) and the NASCAR driver Dale Earnhardt junior (* 1974). Both donated their brains in 2016. Chastain had previously advocated a ban on headers in youth football; Earnhardt has suffered numerous concussions.

CTE in the animal model

In a publication in 2015, animal experiments on rats and mice were used to investigate CTE. For this purpose, traumatic brain injuries were generated in rats by pressure waves via detonations, and in mice traumatic brain injuries were triggered pneumatically. In standardized tests, impulsive behavior and cognitive deficits were then quantified and hyperphosphorylated tau proteins were posthumously analyzed immunohistochemically. The traumatized test animals showed noticeable differences both in behavior and in the tau proteins compared to control animals. Experiments on mice, which were given six mechanical blows to the head for seven days, revealed widespread astrogliosis, activation of the inflammatory cells of the central nervous system and an accumulation of hyperphosphorylated tau proteins six months later . Since these neuropathological phenomena are characteristic of CTE, a first animal model is now available for further CTE analyzes, in particular the pathophysiology of CTE.

literature

  • Pschyrembel - Clinical Dictionary. Walter de Gruyter, Berlin / New York 1994 (257th edition), p. 210 and p. 308.
  • Dominic A. Carone, Shane S. Bush: Dementia Pugilistica and Chronic Traumatic Encephalopathy. In: The Neuropsychology of Cortical Dementias. Edited by Chad A. Noggle and Raymond S. Dean. Associate Editors: Shane S. Bush and Steven W. Anderson. Springer Verlag, New York 2015, ISBN 978-0-8261-0726-8 , e-book ISBN 978-0-8261-0727-5 , Chapter 12. pp. 303–326.

Web sources

Individual evidence

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