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 its like to stand up and suddenly strike your head against something), inside your skull, your brain is probably rattling around.

But it isnt 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. Thats when a concussion or mild traumatic brain injury is likely.

Everyone talks about concussion in sport, but theres more to it than that

Even if theres 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 Dr 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 Universitys 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 biomarkersimaging, [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.

Its 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 theres a loss of consciousness, sometimes there isnt.

Perhaps the greatest diagnostic challenge for both clinicians and patients is that symptoms vary between people.

Diagnosing concussion isnt as straightforward as you might think, says Dr Sarah Hellewell, a neurotrauma researcher from the Peron 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.

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 Alzheimers, Parkinsons, Huntingtons, 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.

CTE is remarkably like Alzheimers. 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 Alzheimers 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.

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At a molecular level, tau tangles appear in different layers of the brain and may have different folded structures between CTE and Alzheimers.

But while Alzheimers 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. Its found in all neurons in the brain and it serves to stabilise their long outward projections called axons, says Buckland.

Its all about how much exposure your brain is getting to these acceleration and rotational forces over short periods of time.

Within those axons is whats 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 Alzheimers 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.

Its not unlike a blood clot obstructing blood flow, except we have neural proteins crammed together in nerve cells.

Technically, both CTE and Alzheimers can only be conclusively diagnosed after death, that is, via a post-mortem examination of a persons brain (although Alzheimers has many clinical symptoms which enables a pre-death diagnosis).

The term mild is attached to TBIs and concussions, but its 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. Thats 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, lets say youve initiated CTE by some event take alcohol, that worsens the pathway the chances of developing CTE go up, its 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

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What happens in your brain when your head gets hit? - Cosmos