The news that legendary St Kilda defender Danny Frawley was suffering from the neurodegenerative condition known as CTE (chronic traumatic encephalopathy) when he died one year ago, is shocking.

Frawley is only the second former player to be diagnosed with CTE, following its initial discovery in the brain of the late Graham “Polly” Farmer earlier this year. The finding has the potential to rock the AFL to its core, establishing an incremental link between head knocks on the field and tragic mental problems later in life.

But what is CTE? What’s the difference between it and concussion? And how are football codes handling the problem?

What is concussion?
Concussion is a transient injury caused by any jolt to the head (or body) that delivers an impulsive shock to the brain, causing it to rock back and forth in the skull or twist on its axis. It’s a functional “neurological disturbance” rather than a structural injury and hides itself well. It will not show up under X-ray or CT scan or MRI, or in tests of blood and saliva.

In fact, concussion is diagnosed only by observing overt symptoms such as dizziness and confusion, nausea and unsteadiness. Complicating matters, the condition varies wildly between individuals and incidents. Symptoms can manifest instantaneously – or appear hours later. And they can linger for months – or disappear within minutes.

OK, so what’s CTE?
Chronic Traumatic Encephalopathy (CTE) is a degenerative brain disease found in people with a long history of head trauma – not so much a handful of big concussions but rather hundreds (or thousands) of smaller impacts over a number of years.

The Concussion Legacy Foundation, the advocacy arm of the ground-breaking concussion research group at Boston University, makes a distinction between bigger hits and “subconcussive impacts” (of the kind sustained when NFL players routinely bang their helmets into one another). The foundation uses the analogy of a car driving down a poorly maintained road. Sure, big potholes might burst a tyre or crack an axle but smaller potholes do immense harm too: drive over those little bumps a dozen times a day, every day of the year, for more than a decade, and the wear and tear can be catastrophic.

It makes sense then that CTE was first diagnosed in 1928 in boxers, under the descriptor dementia pugilistica (also known as “punch drunk syndrome” and later “slug nutty”) but it roared back into the public consciousness in 2005, when pathologist Bennet Omalu found CTE in the brain of an American footballer, former Pittsburgh Steeler Mike Webster. This discovery was subsequently made into a movie starring Will Smith as Dr Omalu (although a recent investigation by the Washington Post – From Scientist to Salesman – calls into question some of Omalu’s claims and motivation).

How do you diagnose CTE?

CTE often manifests as a kind of dementia but can only be diagnosed post-mortem. Once a person who has pledged their brain dies, they are sent to a mortuary where their brain is removed and weighed then fixed in formalin to preserve the tissue.

Researchers scrutinise photos of the brain for bleeding, bruising and patterns of atrophy, where the sulci (valleys) and gyri (bumps) of the brain have become deep or shallow, narrow or wide.

They then slice the brain vertically at three-millimetre intervals along what’s called the coronal plane, photograph each slice and place portions the size of a postage stamp into microscope slides. The slides are washed in various stains that react to proteins and – in the search for CTE – scientists look specifically for the dark brown build up of a protein known as Tau.

“Tau normally helps a healthy neuron,” says concussion expert and neuroscientist Dr Alan Pearce. “But if an accumulation of it clumps, it can strangulate a neuron or nerve cell. Found in specific places, it becomes evidence of a degenerated brain.”

More information may be found at Centers for Disease and Control and Prevention