Fans of the English soccer club West Bromwich Albion hold signs in honor of the late striker Jeff Astle. Photograph by Scott Heavey / Getty

Last week, the New York Times reported that Bellini, Brazil’s team captain in the 1958 World Cup, who died in March, suffered from chronic traumatic encephalopathy, or C.T.E., the degenerative brain disease best known in the United States for its victims among former boxers and N.F.L. players. Bellini was not the first soccer player to have been identified with C.T.E. Last February, Patrick Grange, an American semi-professional player who died in 2012, at the age of twenty-nine, was also found to have suffered from the disease. As a result, the question has been growing, with some urgency this year, as to whether soccer, like other contact sports, has its own brain-injury case to answer.

In England, where I live, and where soccer is a national, multibillion-dollar obsession, we had a chance twelve years ago to get on top of the possible risks of head injury in the game, after Jeff Astle, a legendary striker for West Bromwich Albion, a club in the Midlands, died in retirement at the age of fifty-nine. Astle, a prolific header of the ball, had received a diagnosis of early-onset Alzheimer’s. Following his death, however, a neuropathologist found that he had in fact been suffering from dementia pugilistica, or boxer’s disease, as C.T.E. was then commonly known. In a widely reported ruling, the local coroner attributed Astle’s illness to soccer. The verdict was “death by industrial disease.”

The case caused headlines but little more. England’s Football Association, which has governed the game since 1863, promised a ten-year study into the effects on young players of heading soccer balls. But the study fizzled out, and the story went away. It was only this year, after C.T.E. assumed its high profile in American sports—in 2013, the N.F.L. agreed to pay seven hundred and sixty-five million dollars to settle a lawsuit over concussion injuries brought by more than forty-five hundred former players and their families—that Astle was remembered once again. Earlier this year, Willie Stewart, a consultant neuropathologist at Glasgow’s Southern General Hospital and one of Britain’s leading experts on traumatic brain injury, studied samples of Astle’s brain tissue and diagnosed him with C.T.E. “In terms of head injuries and dementia, in boxers and others that I have seen, it was amongst the worst,” he told me last week. “It was quite a remarkably scarred brain.”

A couple of days after the Bellini story appeared, I called Dawn Astle, Jeff’s daughter. A retired police worker, she had just picked up her daughter from school; she spoke on the phone in her bedroom. With her sister, Claire, Dawn Astle runs Justice for Jeff, a campaign to raise awareness of the dangers of head injuries in soccer, and to care for older players. “Our lives have been completely, completely turned upside down since March,” she said. “I can’t even tell you how much. It’s just madness.” This time, the Astle story has taken hold. Over the weekend, fans at West Bromwich Albion’s game against Burnley stood and applauded in the ninth minute—Astle wore the number 9—in support of the campaign.

Soccer is a sport newly vexed by concussion. This year’s World Cup in Brazil broadcast to an audience of billions the game’s cavalier approach to the risks of brain injury. Several players—including Javier Mascherano, of Argentina; Álvaro Pereira, of Uruguay; and, in the final match, Christoph Kramer, of Germany—played on, or attempted to, after suffering heavy blows to the head.

In August, a group of parents and players launched a class-action lawsuit in California accusing FIFA, the sport’s world governing body, along with U.S. Soccer, the American Youth Soccer Organization, and others, of presiding over an “epidemic” of concussions in the game. The lawsuit claims that roughly fifty thousand high-school soccer players sustained concussions in 2010—more players than in basketball, baseball, softball, and wrestling combined—and demands that limits be placed on the number of times that players under seventeen may head the ball.

All the while, Dawn Astle’s phone has kept ringing. Recently, she received a letter from John Poole, an eighty-one-year-old former goalkeeper for Port Vale, a club in the third tier of English soccer, with the names of twenty fellow-players who he knew had been given a diagnosis of Alzheimer’s. “Twenty names,” she said. “From one guy. From one team.”

Not everyone wants to listen. Like American football, like wrestling, like ice hockey, like rugby, soccer is following its own particular playbook of denial, anger, and bargaining when it comes to brain injuries. “This is ‘Groundhog Day’ with each sport, each time this comes up,” Willie Stewart told me. In England, the standard argument is that the game is different now: it’s less violent, the balls are lighter, the medical staff are better trained. But none of these claims is backed with proof. Modern soccer balls weigh between 14.5 and sixteen ounces. During even amateur games, they can travel at fifty miles per hour. “Guys are playing harder, playing faster, committing more,” Stewart said. “There is nothing to suggest that the game has gotten better, because, quite frankly, they have never bothered to gather the data looking at the problem in the first place.”

Data is the challenge. C.T.E. can be conclusively diagnosed only after death, and there is an acute shortage of confirmed cases across all sports. In a country in which an estimated two million people play soccer each week, Astle’s brain is still the only one from a former player that Stewart has examined. Then there is the complex, and still largely mysterious, mechanics of how blows to the head can trigger a long-term deterioration of the brain. According to Stewart, the intense recent publicity around C.T.E., and the hectic pace of research in the field, might be tempting neuroscientists to group a range of possible pathologies and dementias under a single label.

“Alzheimer’s disease was the only dementia that people recognized for many, many years,” Stewart said. “Now we are recognizing a whole bunch of dementias in there. I think C.T.E. is head-injury-associated dementia, but there might be varying presentations of it, and varying pathologies of it.” For instance, he said, the accumulation of tau proteins, which become toxic to the brain, is often seen as the telltale sign of C.T.E., but this focus might overlook other symptoms, such as chronic inflammation, the buildup of amyloid proteins, and the degeneration of white matter. “It’s not just the tau,” he said. “There are other things happening as well.”

And C.T.E. isn’t the only concern; milder head injuries also affect the brain in various ways. This has particular relevance for soccer. While it shares with other contact sports the occasional big, obvious collision, soccer also delivers persistent, deliberate, subconcussive blows to the skull as players pass, control, and attack the ball with their foreheads. “It’s a very complicated biomechanical problem,” Michael Lipton, of the Albert Einstein College of Medicine, told me. “It is a matter of which direction is the ball coming, where is the head? What’s the angle of impact? What was the neck-muscle strength? Did the person know it was coming? Did they stiffen? Did they whip their head around?”

Unsurprisingly, early indications are that lots of heading isn’t particularly good for you. In a study published in September in the journal Radiology, Lipton and a handful of his colleagues examined the brains of thirty-seven amateur soccer players in New York. The players had accrued between thirty-two headers and an estimated fifty-four hundred in the previous year; the study put the median at about four hundred and thirty, which works out to eight or ten headers a week. Those who had headed the ball the most did the worst on a series of standard cognitive tests. Their brains also showed lower fractional anisotropy, a measure of the structural coherence of white matter. “Everything really converged to say that the more heading you did, the worse your brain looked,” Lipton said. He stressed that these were preliminary findings. He also stressed that this wasn’t about finding a connection with C.T.E. “That is not the point at all,” he said. “The question is: How different are you than you would be if that had not happened? Or, to make it sound really horrible, let’s say you have a twelve-year-old child playing competitive soccer and heading. What is the expected cognitive or behavioral trajectory of that kid? And how is that altered or impeded by this exposure?”