‘Concussion is a red herring’ for CTE: Major study shows repeated hits (even mild ones) are the REAL problem

By Mario Tacher on Jan 18 in Health.

  • Boston University has found the biggest problem for CTE is the way the head is hit, not the concussion
  • Concussion is to CTE what a cough is to lung cancer: it does not predict it and treating it does not prevent it
  • The paper is the clearest evidence to date of a causal link between football tackles and CTE – and suggests there is no way to prevent it 

Concussions do not cause long-term neurological disease – it is repeated exposure to tackles, even mild ones, that wreck the brains of athletes such as football players and boxers, a major new study has found.

The groundbreaking paper published today by the same Boston University team that diagnosed disgraced former Patriots star Aaron Hernandez with CTE last year is the first to show how sports tackles directly cause the devastating brain disease, which causes aggression, dementia and suicidal thoughts.

Testing mice, they showed that repeated blows to the head trigger the wasting disease within 20 minutes, whether the mice suffered a concussion or not.

Simply put: concussions are to CTE what a cough is to lung cancer. A cough does not predict lung cancer, and treating it does not prevent or cure lung cancer. It is the same for CTE.

And it brings into question a Supreme Court ruling last year that said players need documented concussions to collect compensation from the NFL’s brain injury bank.

The concussion is the red herring here,’ lead author Dr Lee Goldstein, associate professor at Boston University, told Daily Mail Online.

‘This is the strongest evidence to date of a causal linkage between hits in football and CTE. We can probably prevent concussion. But what we can’t do is prevent the motion of the head from a tackle. And that’s the real problem.’

Dr Goldstein, an associate professor at Boston, authored a major report in 2012 about soldiers, showing exposure to even one bomb blast can cause CTE.

His new paper published today has shown the same is true for head hits in sports.

‘It is not the concussion, it is the way the head is hit’ Dr Goldstein explains.

‘At the end of the day, there is no difference in the way brain looks after a hit, no matter how the hit was sustained. Any hit can have this effect. We were not expecting that.

‘This is concerning for everyone, including kids.’

The paper provides the strongest evidence to date that many players with invisible brain injuries from tackling have a significant risk of developing neurodegenerative disease – especially if they have been playing tackle football since childhood, as most NFL players do.

It suggests the current attempts to protect players – by monitoring concussions – may be futile.

Chronic traumatic encephalopathy (CTE) is a degenerative brain disease that is caused by repeated hits to the head.

Over time, these hard impacts result in confusion, depression, dementia, explosiveness, aggression, and suicidal thoughts.

But until now, many believed the harder the hits, the worse the risk of disease.

The NFL has resisted fully participating in the investigations into football’s CTE risk – even cutting ties with the National Institutes of Health project last year after a bitter dispute over investigators being ‘too critical’.

Despite vowing in 2012 to invest $30 million in brain injury research, the football league only paid $18 million, and executives declined to renew when its contract expired at the end of August.

The move came two years after a huge row between the two organizations over Boston University neuroscientist Robert Stern, who is a vocal critic of the NFL and received a chunk of the NIH grant to examine former players.

Just days before the NFL and NIH announced the end of their partnership, Dr Stern’s research team published the explosive report, revealing 110 out of 111 deceased NFL players had signs of CTE in post-mortem examinations.

However, as mounting research has drawn links between football and a host of neurological diseases – including dementia and ALS – the league has been more vocal about recording concussions and offering compensation.

Players who suffer major hits on the field are carted off for a concussion assessment and usually sidelined from play if a concussion is found.

But according to Dr Goldstein, it is the head movement, not the result. Anyone who suffers a blow to the left side of their head, as happens in a bomb blast, has a high risk of developing the dangerous plaques that then grow into neurological disease.

He cites the case of Tom Savage, the Houston Texans quarterback, who suffered a seizure on the field in December after a flying tackle from Elvis Dumervil of the San Francisco 49ers. After a brief stint on the sideline, Savage was put back out to play.

‘He was not concussed. He had a post-traumatic seizure, which was worse. He had a bonafide seizure which was way way worse. And they put him back in. ‘

Dr Goldstein also cited the most famous hit in boxing history, from Rocky Marciano against Joe Walcott in 1952. One blow to the side of Walcott’s face left his right side completely weak and he was wobbling.

The only way to prevent CTE, he says, is not to play football or boxing or any sport that inflicts such head injuries.

‘The biggest risk factor is repeated exposure,’ Dr Goldstein said.

‘You want to know how to prevent it? Don’t play. No helmet can prevent this.’

There is still no approved way to diagnose CTE in humans during life. Despite all the posthumous studies, as well as Boston’s work to identify a biomarker, Dr Goldstein and his colleagues including Robin Cleveland of Oxford University had to use mice to prove the causal relationship.

‘We could assess the animal’s concussion signs immediately after it had been sustained,’ he said.

‘When you moved the head just like we did in the blasts, what we see is a neurological syndrome that doesn’t resemble concussion. A child could tell the difference.’

Boston’s ongoing investigation into football-linked brain injury is studying hundreds of former players’ brains, including Aaron Hernandez, Junior Seau, Dave Duerson, and Andre Waters – all of whom committed suicide and had CTE.

Seau and Duerson both shot themselves in the chest with the expressed intention of donating their brains to scientists to examine them for disease.

As expected, tests subsequently showed that both men and Waters, who were all over the age of 40, had CTE. Hernandez, however, was in his mid-20s – with a far more severe pathology.

Researchers are still unclear on how CTE affects behavior, but a growing swell of studies is offering some answers.

  • CTE sufferers have clumps of tau protein built up in the frontal lobe, which controls emotional expression and judgment (similar to dementia)
  • This interrupts normal functioning and blood flow in the brain, disrupting and killing nerve cells
  • By stage 3 – i.e. Hernandez’s stage – the tau deposits expand from the frontal lobe (at the top) to the temporal lobe (on the sides). This affects the amygdala and the hippocampus, which controls emotion and memory

It is a chilling reality that Dr Goldstein said he can no longer ignore, as his research into CTE and head injuries has deepened.

Now, even attending football games at his daughters’ school makes him feel uneasy.

‘In any other setting I would be mandated by law to report this as child abuse. These children are getting hit on the head repeatedly, and I know it is putting them at risk of neurological disease,’ he told Daily Mail Online.

‘But instead here I am with all the other parents cheering because our team did a good tackle.

‘Kids can’t drink alcohol until a certain age, they can’t drive until a certain age, and they can’t walk around the street hitting each other in the heads with pipes. Those activities can all be lethal. And so can this. There must be a policy change, we have a moral obligation to protect children – and adults – from harm.’

Aaron Hernandez had the most severe CTE case ever seen: Scientists found 27-year-old’s brain tissue showed extreme damage to memory and impulse control

The neuroscientist who analyzed Aaron Hernandez’s brain confirmed that he suffered the worst case ever seen in someone so young, with severe damage to regions that affect memory, impulse control and behavior.

The 27-year-old former New England Patriots player killed himself in April 2017 while serving life in prison for murder.

In September, Dr Ann McKee of the CTE Center at Boston University posthumously diagnosed Hernandez with chronic traumatic encephalopathy, a football-linked disease that causes dementia and aggression.

 

She formally presented her findings a month later, and confirmed that she had never encountered such extreme degradation in a young brain, pointing out areas of severe tissue damage and microbleeds likely caused by blows to the head.

They also found a variant of the APOE gene, which has been linked to increased risk of Alzheimer’s, but the scientists emphasized that no gene could inflict the same damage as years of heavy impact from tackling.

Dr McKee says she could not say for certain that Hernandez’s criminal and suicidal acts were a result of his severe case of CTE, nor whether other 27-year-old players could plausibly have the same pathology. But she says Hernandez suffered substantial damage to several important regions, including the frontal lobe.

‘In this age group, he’s clearly at the severe end of the spectrum,’ McKee said.

‘There is a concern that we’re seeing accelerated disease in young athletes. Whether or not that’s because they’re playing more aggressively or if they’re starting at younger ages, we don’t know. But we are seeing ravages of this disease, in this specific example, of a young person.’

Hernandez was diagnosed with stage three out of four, with four being the most severe.

 

 

 

 

 

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