IN NOVEMBER 2022, a young woman called Heather Anderson killed herself at an army barracks in Perth, Australia. Anderson was a former Australian Rules footballer who had been struggling with depression. Her family donated her brain to the Australian Sports Brain Bank, which confirmed what everyone suspected: Anderson had chronic traumatic encephalopathy (CTE), a degenerative brain disease linked to repeated blows to the head. She was the first professional female athlete to be diagnosed with this condition. She won’t be the last.
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Strange as it may seem, it has taken almost a century to get to grips with what a blow to the head really means. Most people are familiar with concussion, but now we know that even mild knocks to the head can cause long-term problems. “It is misleading to assume that when the physical force applied to the head is weak, the consequences will be less,” says Allison Reiss at New York University.
These consequences are playing out primarily in professional athletes, several of whom are living under the shadow of CTE. Recently, we have seen many of them take legal action against governing bodies. But it isn’t just athletes who are at risk. Even a single blow to the head can put a person in danger of future cognitive problems.
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Thankfully, alongside the harms, there is a growing understanding of what happens to the brain after a knock, which is providing new targets for novel treatments together with a plethora of new technologies that aim to protect people from its devastating effects.
Concussion, or a mild traumatic brain injury (MTBI) as it is formally known, is defined as a transient impairment of cognitive function after a head injury that can’t be picked up by a CT scan. Sometimes, it includes a brief loss of consciousness and memory loss. A blow to the head like those that can be inflicted during a boxing match or contact sports causes the brain to slosh back and forth inside the skull like a gel in a mixing bowl, inflicting physical damage at the site of impact and on its opposite side. However, a blow isn’t necessary to develop concussion – a combination of rapid acceleration, deceleration and rotation of the head, as is commonly seen in traffic accidents, is enough, says Elizabeth Sandel at the University of California, Davis.
According to figures from Norway, of the country’s population seek emergency medical attention for an MTBI every year, mostly after a fall, a sports-related collision, a traffic accident or violence. That, however, is likely to be an underestimate of the true numbers as most people don’t go to hospital, says at the University of Gothenburg in Sweden. The true incidence is thought to .
Long concussion
We know that MTBIs don’t have to be repetitive to lead to long-term problems and it would be wrong to assume that “mild” injuries mean trivial outcomes. For reasons that aren’t well understood, even a gentle blow can cause prolonged and debilitating symptoms. Most people with a one-off concussion recover within three weeks, but . Their symptoms are varied and long term: migraine-like headaches, dizziness, fatigue, aversion to noise and light, blurred vision, flashing lights, neck pain, emotional volatility, depression, anxiety, memory problems, brain fog, insomnia, lower tolerance to alcohol and a preoccupation with the fear that permanent brain damage has occurred.
This so-called long concussion can lead to significant disability and a much-reduced quality of life, according to at Harvard Medical School (see “What is long concussion?”, below.
Things get even worse when people experience repeated bangs to the head. Increasingly, it appears that for some, CTE is the inevitable consequence.
There is a long history of CTE in contact sports. In 1928, a doctor called Harrison Martland published an article in , which fans and promoters called being “punch-drunk”. Early signs were a staggering gait and mild mental confusion similar to being intoxicated; some fighters progressed to dementia. Martland suggested, unsurprisingly, that punch-drunkenness was caused by serial blows to the head. A few years later, the condition acquired a grand Latinate name, .
For many years, dementia pugilistica was regarded as a problem confined to boxing, but in 2005 a hammer blow landed. , then at the University of Pittsburgh in Pennsylvania, and his colleagues , who died suddenly aged 50 after experiencing cognitive impairment, mood changes and Parkinson’s-like symptoms.
That set off a cascade of events that continues to play out today. On 17 February 2011, former Chicago Bears player David Duerson killed himself at his home in Florida. Prior to his suicide, he sent a text message to his family instructing them to donate his brain to Boston University School of Medicine, where researchers were studying CTE. They posthumously diagnosed him with the condition. A year later, another former footballer, Junior Seau, also died by suicide. In 2013, more than 4500 former athletes sued the National Football League (NFL) for concussion-related brain injuries and won $765 million in damages. In December last year, hundreds of former professional rugby union players initiated legal action against World Rugby, the Rugby Football Union and the Welsh Rugby Union claiming that these bodies had failed to put in place any reasonable measures to protect their heads.
A spokesperson from World Rugby says on behalf of all three organisations: “The whole of rugby cares deeply about all of our current and former players, we will never stand still when it comes to player welfare. While we cannot comment on the ongoing legal action whilst we wait for the claimants to set out their arguments in full, nor reach out to the players involved directly, we would want those players to know that we listen, we care and continue to champion player welfare as the sport’s number one priority.”
Concussion and CTE
CTE is a problem that won’t be going away any time soon. Last year, researchers at Boston University reported that , though they warned that this doesn’t reflect the prevalence among ex-players as not all of them donate their brains to science. But it does suggest there is something very wrong: prevalence in the general population is extremely low, under 1 per cent. CTE has also been diagnosed in wrestlers, ice hockey and baseball players, a professional , a cyclist, military personnel exposed to blast injuries and people who have experienced domestic abuse.
Despite initial doubts about the cause of CTE, there is now clear evidence that it comes about through repeated blows to the head. More than 97 per cent of published cases of CTE are in people with a known history of repetitive head impacts, mostly from contact sports, according to Ann McKee at the US Department of Veteran Affairs in Boston. Empirical evidence backs this up. A recent study by , now at the University of Glasgow in the UK, and his colleagues found that professional soccer players who headed the ball more and had longer careers were more at risk of CTE. He and his team have also found that . “No game which involves repetitive head injury can be immune to this,” says Stewart.
Women at higher risk of concussion
Sportswomen may be at even higher risk than their male counterparts. In soccer, for example, women report , perhaps because their neck muscles are generally weaker. Women also seem to endure more severe symptoms for reasons that aren’t well understood.
While CTE tends to only be diagnosed post-mortem, by tell-tale tangles of an abnormal brain protein called tau in the cerebral cortex, it causes a range of symptoms in the living. These include disorders of cognition, mood, behaviour and movement and, in severe cases, dementia. But diagnosis is difficult, as these symptoms have largely been identified from interviews with people who knew deceased individuals diagnosed at autopsy with CTE. They can also be difficult to distinguish from mental health conditions and post-concussion symptoms. Blood and neuroimaging tests are in the pipeline, according to McKee, but in the meantime diagnosis is a bit hit and miss.
Treatments for CTE
Symptoms of CTE can be managed, but . There is, however, an increasing understanding of the neurological changes that occur after repetitive head injuries, which may offer targets for early intervention. They come in phases, a cascade of destruction that plays out over days, weeks and even years.
The first phase is excitotoxicity, caused by the release of chemicals from ruptured brain cells. The main culprit is glutamate, a neurotransmitter that activates receptors on other neurons. This principally causes neurons and support cells to become more permeable to calcium, which floods in and initiates a wave of destruction. Calcium-swamped cells activate various enzymes that attack membranes, proteins and DNA, leading to mass cell death.
The enzymes also attack mitochondrial membranes, causing these energy-producing organelles to disintegrate, setting off phase two, oxidative damage. This causes violently reactive compounds, which are usually sequestered inside mitochondria, to leak out. The concentration of these dangerous compounds can stay high for days. Phase three is neuroinflammation, which is quickly followed by a final round of cell death.
This final phase may offer the best target for treatment via inhibition of a class of enzymes called caspases, which are the main cause of cell death. and may eventually be ready for use in humans with MTBIs, according to Reiss.
For now, the focus is on prevention, and there are several emerging measures that aim to reduce the risk. Many contact sports now have on-field procedures to diagnose and remove players with concussion, not just for professionals . Around the world, both amateur and professional soccer players are being trained , and some federations have banned heading altogether from youth soccer.
Smart mouthguard
Technology is also playing its part. In October last year, World Rugby debuted its “smart mouthguard” in an international women’s rugby match, before rolling it out for players in this year’s Six Nations tournaments. The device monitors accelerations and flags any above set thresholds to medics. The player is taken off and assessed and, if need be, kept off. Flagged players may also be monitored after the game. This is the first of a raft of new technology that is likely to be a permanent fixture in future seasons. Researchers at the University of California, San Francisco, , while Stanford University in California is working on an .
Of course, the safest way to avoid the potentially horrendous complications of head injuries is to avoid head injuries altogether. In 2021, the and Stroke agreed on how to diagnose CTE while a person is still alive. The leading criterion is “substantial exposure” to repetitive head injury.
Stopping playing the sport you love or depend on for your income will never be an easy decision. But if head injuries are a risk you routinely take, it is well worth doing everything you can to protect yourself.
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What is long concussion?
The fact that some people with concussion don't recover in the expected time frame has been recognised for decades. The term "post-concussion syndrome" was first proposed in 1934, though it remained controversial for many years, in part because there was a perception that people were faking it in search of compensation.
But recently, post-concussion syndrome – or "long concussion" as it is often called – has risen up the medical agenda, propelled in part by the attention paid to chronic traumatic encephalopathy (see main story).
In 2019, researchers representing the called for a paradigm shift in the way that people are treated and managed, starting with a rebranding. "Post-concussion syndrome" suggests intractability, they argued, which isn't true. Better to call it "persistent symptoms after concussion (PSaC)" instead. At the same time, there has been a shift away from passively waiting for symptoms to disappear to active intervention, according to at the Danish Concussion Center in Copenhagen.
There are many challenges to understanding long concussion. For a start, not everybody has the same set of symptoms, and many people who are ill with something else, such as chronic pain, anxiety or post-traumatic stress disorder, can have very similar ones. Such overlaps create a "fundamental challenge" in defining the disease, says Grant Iverson at Harvard Medical School. There is also a lot of uncertainty around why some people with concussion go on to develop long-term symptoms, while others don't. Iverson describes it as a "conundrum".
We are making headway, though. Research from the 1990s found that personal setbacks prior to the injury, such as financial hardship or problems at work, can predispose people to PSaC. More recently, at the NTNU Faculty of Medicine and Health Sciences in Trondheim, Norway, assessed 378 people on a range of factors prior to their injuries to see if certain individuals are at greater risk. She found : being female, having a history of headaches and other pain, being unemployed or underemployed, having a neurotic personality type and low resilience, sleeping poorly and having symptoms of ADHD.
Again, why these predispose some people to PSaC isn't known, but it does offer the opportunity to intervene early when vulnerable people have a mild traumatic brain injury.
Graham Lawton is a features writer at żěè¶ĚĘÓƵ
