Verge: FIGHTING DIRTY - Behind boxing's brain damage crisis

At 46, "Terrible" Terry Norris has the lean, muscled frame of a former pro boxer. He’s just a little taller than average, with a thick, black Van Dyke framing a bright smile. Gray creeps in at the edges of his beard, but his shaved head seems the only concession to age, a paring away of the intricately razored box cut of his heyday, now some 20 years gone. These days, he teaches cardio boxing in a converted garage north of Hollywood; upstairs, he shares a loft with his wife, Tanya, who also teaches and runs his gym. During classes he looks fit and powerful, his fists still preternaturally fast. Only when he speaks, in a low, raspy murmur bordering on unintelligible, do you wonder at the damage he’s suffered.

When the NSAC refused Norris’ fight license, it hoped to prevent him from following the path of Muhammad Ali, Jerry Quarry, Floyd Patterson, and Sugar Ray Robinson — all legends of the sport struck by post-career brain illnesses, and whose decline played out with varying degrees of publicity. Aging boxers have long suffered increased risk of mental health issues, from Alzheimer’s to Parkinson’s syndrome to dementia pugilistica; these afflictions have been largely accepted, if quietly and perhaps without reflection, by fans and fighters as potential consequences inherent to the sport. Yet today, as professional football begins to face its own reckoning over brain-damaged players, boxing is receiving new scrutiny from researchers hoping to understand just what happens inside a boxer's brain during a career. And that means understanding men like Terry Norris.

What he saw shocked him. At the microscopic level, Webster’s brain had become a riot of black and brown skeins: deposits of a modified protein called tau. Tau normally lines the inside of the nerve cell, providing stability, but here had built up in what’s called neurofibrillary tangles. When Omalu later published his findings, those tangles became the calling card of CTE.

Scientists don’t yet know how a series of mild traumatic brain injuries becomes CTE, largely because it’s nearly impossible to see accumulated tau proteins until after death. So diagnosis depends on clinical judgement and a careful reading of patient histories. Early on, CTE can usually be distinguished from other types of dementia, but later stages are more difficult to identify. The three categories of symptoms — cognitive, mood, and behavior — each carry frustratingly difficult questions. For example, when does forgetfulness cross into diagnostically relevant changes in cognition, like memory impairment and problems with planning, organizing, multitasking, and judgement? When do depression, apathy, and irritability indicate early CTE and when are they signs of other mental illnesses? What about problems with impulse control, substance abuse, aggression, and violence?