When you hit your head – or when something hits it – your brain is going to feel it.
While that thud might trigger a pain response (we all know what it’s like to stand up and suddenly strike your head against something), inside your skull, your brain is probably rattling around.
But it isn’t just a strike to the cranium that causes your grey matter to rock back and forth: concussions occur when the body – anywhere on the body – is impacted such that the head, and the brain within it, suddenly moves.
If the effect of this biomechanical force is enough to cause the brain to hit against the skull, or twist, physical and chemical damage may occur to the neurons – brain cells – that are essential to its normal, healthy function. That’s when a concussion or mild traumatic brain injury is likely.
Even if there’s no clinical diagnosis of concussion, the potential for subtle, silent, mild TBI remains.
“We know from accelerometer data… that the head undergoes quite a lot of significant acceleration/deceleration events [in sport],” says Associate Professor Michael Buckland, the head of the neuropathology department at the Royal Prince Alfred Hospital and Executive Director of the Australian Sports Brain Bank at Sydney University’s Brain and Mind Centre.
“Only a small minority of those lead to clinical signs and symptoms that would be diagnosed as concussion – the vast majority appear to be clinically silent.
“But there is evidence, if you look at circulating biomarkers…imaging, [and] advanced MRI studies after a game of sport, that there is actually a subtle traumatic brain injury or settled damage to the brain from those events, even though you feel completely fine.
“It’s all about how much exposure your brain is getting to these acceleration and rotational forces over short periods of time.”
A concussion or mild TBI might be accompanied by a range of symptoms, from headaches, nausea and sensitivity to sound or light, to memory problems, brain fog, sleep problems and heightened emotions.
Sometimes there’s a loss of consciousness, sometimes there isn’t.
Perhaps the greatest diagnostic challenge for both clinicians and patients is that symptoms vary between people.
“Diagnosing concussion isn’t as straightforward as you might think,” says Dr Sarah Hellewell, a neurotrauma researcher from the Perron Institute and Curtin University, in Perth.
“There are various guidelines, but mostly diagnosis is based on reports from patients themselves or people around them at the time of injury. Most guidelines or tests include criteria such as presence of symptoms, alterations in mental state, the time of loss of consciousness or amnesia, if any.”
The Trouble with Tau
In the simplest terms, neurodegeneration occurs when neurons in the brain deteriorate. Repeated concussions without adequate recovery might play a major role in this process.
Too much cell death and dysfunction could lead to any of several pathologies, including Alzheimer’s, Parkinson’s, Huntington’s, motor neurone diseases, and amyotrophic lateral sclerosis (ALS).
CTE – or chronic traumatic encephalopathy – is in there too, and that has captured the concerns of the sporting community in recent years.
“Mostly diagnosis is based on reports from patients themselves or people around them at the time of injury.”Dr Sarah Hellewell
CTE is remarkably like Alzheimer’s. Both show shrinkage in the hippocampus, which plays a crucial role in learning and processing information as part of short and long-term memory formation. Change to the hippocampus is associated with a range of neurodegenerative and psychiatric disorders.
Both CTE and Alzheimer’s appear to share a common problem: toxic tau. Tau proteins play an important structural role in stabilising microtubules in brain axons – the long cable-like structures of neurons that extend away from the cell body, ending in the synapses used to communicate with other brain cells.
Trauma to the brain causes tau proteins to clump together in tangled masses and alter normal brain functioning.
At a molecular level, tau tangles appear in different layers of the brain and may have different folded structures between CTE and Alzheimer’s.
But while Alzheimer’s might be triggered by several age, genetic, environmental and lifestyle factors, CTE is found in those with histories of repeated impacts to the head.
“Tau is actually a normal, cellular protein. It’s found in all neurons in the brain and it serves to stabilise their long outward projections… called axons,” says Buckland.
“It’s all about how much exposure your brain is getting to these acceleration and rotational forces over short periods of time.”Associate Professor Michael Buckland
“Within those axons is what’s called microtubule associated protein tau or MAPT [pronounced Map-Tee], and the tau stabilises the microtubules to give structural integrity to that axon.”
“In CTE, as in Alzheimer’s disease, the tau takes on an abnormal shape, gets abnormally modified chemically – a lot of phosphorylation is added to it – and it tends to move out of the axon and clump in the nerve cell body.”
Buckland explains that many neurodegenerative diseases appear to be characterised by this abnormal accumulation of wrongly folded proteins.
It’s not unlike a blood clot obstructing blood flow, except we have neural proteins crammed together in nerve cells.
Technically, both CTE and Alzheimer’s can only be conclusively diagnosed after death, that is, via a post-mortem examination of a person’s brain (although Alzheimer’s has many clinical symptoms which enables a pre-death diagnosis).
The push for better post-injury care
The term mild is attached to TBIs and concussions, but it’s deceptive – no brain injury is truly mild and there is need for close monitoring of the individual athlete.
A tennis player enduring their first nausea-inducing head hit might be fit and firing after two weeks, but a footballer placed on their fifth concussion stretcher might need much, much longer to heal properly. The brain can recover, but subsequent trauma which occurs before that process has been completed is what worries scientists: does repeat injury before recovery compound the problem?
“If you subject your head to repeated concussion, you increase the chances that you might have a long-term brain disease. That’s not rocket science,” says Emeritus Professor Robert Vink, a neuroscientist from UniSA.
Risk reduction in the immediate aftermath of a mild TBI or concussion is, therefore, crucial – not just for short-term recovery but to reduce long-term risk.
For example, Vink warns about post-concussion drug and alcohol consumption.
“Drugs worsen the CTE pathways. So, let’s say you’ve initiated CTE by some event – take alcohol, that worsens the pathway… the chances of developing CTE go up, it’s another insult to the brain on top of the head knock,” Vink says.
48 hours abstaining from drug and alcohol consumption, rest and monitored sleep, and avoiding strenuous activities like reading, television and screen use are among the current best practice care recommendations from Connectivity, a leading brain injury awareness organisation in Australia.
Understanding the physical and chemical changes that take place within the brain is crucial in the quest to provide clarity and information to communities around mild TBI and concussion: what it is, how to manage it, and when a person can return to participate in the activities they love.
When it comes to the sudden impact of biomechanical force on the brain, few, if any, sports are spared. Now science is revealing the potential extent of repeat head injury, codes are mobilising to respond.
But athletes, and the communities around them, also need definitive diagnosis of brain injuries, their seriousness, and to be given clearer management plans to ensure safe recovery.
To achieve this, neuroscientists are chasing elusive but hugely powerful biomarkers that could make the diagnosis and management much, much more effective.
Next week: The hunt for brain injury biomarkers
Editor’s note: We have updated the position title for Associate Professor Michael Buckland
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