Kevin Turner was a premier athlete in the National Football League, a fullback who could run, catch and block. At 6' 1" and roughly 230 pounds, he was slightly undersized for his position, but he had tremendous thrust in his legs and used all of it to launch himself into players who were bigger than he was. He played for the New England Patriots from 1992 to 1994, then joined the Philadelphia Eagles, with whom he stayed until his abrupt retirement in 1999. Some called him “the Collision Expert”—a nickname he got because of the gouges he collected on his helmet.

Now Turner can’t button his shirt. When we met recently at a California Pizza Kitchen in Birmingham, Ala., the first sign of physical impairment came when he put his small backpack into the booth where he would be sitting. His arm was Frankenstein-straight, and his shoulder was stiff as he swung the pack away from his body. Other issues soon became apparent. His fingers were curled up and his thumbs almost useless, so he drank from a glass by holding it in his palms. After he had trouble removing the little paper ring from his napkin, he took a furtive glance at the nearby tables before ducking his head down to rip it off with his teeth.

“I can’t tell you how frustrating it is to open a box of cereal,” the 42-year-old father of three told me as we left the restaurant. “Opening a box of cereal is an event.” Turner needs someone to help him pull his pants on in the morning. His then 11-year-old daughter performed that duty the day I met him. She also helped him shave.

In 2010 Turner was diagnosed with amyotrophic lateral sclerosis (ALS), commonly known as Lou Gehrig’s disease. Nobody knows what causes ALS. In 5 to 10 percent of cases, the disease is inherited; otherwise, it is a random death sentence. Its arrival is a mystery, and there is no cure.

Now a group of scientists in Boston believes that Turner, despite suffering symptoms of ALS, may not really have the disease. Around the same time he was diagnosed, these researchers discovered what they say could be a separate disorder with exactly the same clinical syndrome as ALS. It is also incurable. The only real difference is that this disease seems to have a clear cause: repeated blows to the head, like those that often occur on the football field.

The finding is hugely controversial. Many specialists in ALS have been critical of the science behind the new study and worry that it has confused their patients. They maintain that decades of research trying to find a link between head trauma and ALS have been inconclusive at best. They have been particularly incensed by the suggestion, made in press interviews, that Lou Gehrig might not have had Lou Gehrig’s disease. In a letter to the editor of the Journal of Neuropathology & Experimental Neurology, more than a dozen doctors and researchers questioned the science in the findings and complained that “many patients have understandably been frightened and confused by these statements and are now wondering if their diagnoses are correct.”

Ann McKee, a neuropathologist at Boston University and the Bedford VA Medical Center in Massachusetts, is the primary scientist behind the study. She says she regrets the controversy stirred up by the speculation regarding Gehrig but stands firmly behind the science. Her original study was based on three cases, and she now has five more, as well as three other suspected cases awaiting confirmation. McKee and her colleagues liken their battle to the one waged by scientists trying to show that smoking causes cancer. There has been a lot of resistance, but ultimately, they believe, they will prevail in showing that repetitive concussions cause a motor neuron disease with ALS-like symptoms.

Already findings about the potential for repetitive concussions to cause other forms of mental impairment have spurred the NFL to change some of its rules on flagrant hits to the head, and many states have passed legislation to ensure that young athletes do not return to the field too quickly after a concussion. Even some scientists critical of certain details in McKee’s research, or the way in which it was presented to the press, believe her findings are significant. “The core observations of her work are very important,” says Robert Brown, chair of neurology at the University of Massachusetts Medical School, “and the public policy implications are staggering.”

Havoc in the Brain
To grasp the controversy, it helps to first understand what happens inside the brain when someone suffers a concussion. Our current knowledge is based largely on animal models—experiments on rodents and cats—as well as the monitoring of human patients in intensive care with severe brain injuries and magnetic resonance imaging of people with mild concussions. Part of this picture is uncertain, but the science is improving. “Previously there was no way to get some of the necessary data without drilling a hole in somebody’s head,” says Christopher Giza, an associate professor of pediatric neurology and neurosurgery at the University of California, Los Angeles, who has done a review of the scientific literature. “We now have advanced imaging that has provided us with some of this information.”

What is clear is that when the head, moving at significant speed, comes to an abrupt stop, the brain cells inside get stretched, squeezed and twisted. In their normal state, these cells function by transmitting electric current. A part of the cell called the axon acts somewhat like a wire, conducting current between the cells. Ions shift back and forth along the axons in a controlled fashion, transmitting messages from one part of the brain to the other and to the rest of the body. When a concussion occurs, however, the membranes of brain cells get damaged and the cells become leaky, Giza says. Ions rush in and out indiscriminately. As sodium and calcium rush in, potassium rushes out. The brain needs to restore balance.

When I asked Giza if he could compare this process to a car wreck, he said a submarine or boat accident would be a better analogy: leaks are springing everywhere, and emergency crews struggle to keep up. In the injured cells, microscopic pumps try to get the ions back in their proper places. The pumps require energy, however, and the stressed cells face an energy crisis. At the same time, other havoc is taking place. When ions rush in, they tend to destroy the scaffolding of the cell. “It’s as if someone is in there with a saw, cutting through all the struts and supports,” Giza says. Calcium inside the cell, moreover, can activate enzymes that can trigger the cell to destroy itself.

In severe cases, some brain cells simply break apart under the stress. In milder cases, which Giza calls “sublethal,” there is an opportunity to recover. How long that recovery process takes is uncertain. In rats, it takes roughly a week to 10 days. But time­scales are generally longer in humans than in lab rats, which have a life span of only about two years. A human brain may take longer to return to a normal, healthy state.

So what happens if, in the middle of the emergency recovery process, the brain suffers another concussion—or several more?

From Concussions to Brain Disease
It has long been clear that multiple blows to the head can lead to mental impairment. Boxers refer to this breakdown as becoming punch-drunk. But it is only in the past decade that scientists have identified the problem in American football players. They have also been able to identify, on autopsy, pathological markers for the disease, now called chronic traumatic encephalopathy (CTE).

Some scientists still doubt or deny that former NFL players are suffering severe depression, memory loss, erratic or aggressive behavior, and early dementia because of repeated blows to the head. Yet a disturbing number of former NFL players have committed suicide or died after suffering mental disturbances, and many of them, worried that they have the disease, have arranged to donate their brain to science. One of the more recent was David Duerson, a former star safety with the Chicago Bears, who shot himself in the chest (not the head) and left instructions to give his brain to the NFL brain bank for study. As in many other cases, an autopsy determined that Duerson had CTE.

McKee is one of the scientists at the forefront of this research. She performed Duerson’s brain autopsy and oversees a total brain bank of more than 100 donations, around 30 of them from former NFL players. Her morgue at the Bedford VA center has seven stainless-steel freezers loaded with frosty buckets of brain matter. When newly donated brains come in, McKee conducts autopsies and examines bits of brain tissue under a microscope. She looks mainly for abnormal deposits of two proteins: tau and TDP-43. The remaining brain matter is frozen and stored at –80 degrees Celsius (–112 degrees Fahrenheit) so it can be used for other research.

On a recent tour of the facility, McKee showed me two newly received brains. They looked like gelatinous hunks of coral or some other bottom-dwelling sea creature. Dressed in a blue vinyl smock and white rubber gloves, McKee turned one of the brains over and around in her hands, then delicately sliced off a piece the size of a fingernail and placed it in a plastic cassette. Bits of the tissue would later be stained for tau, TDP-43 and other markers. On the wall was a list of 28 regions of the brain that should be tested, but McKee said the actual list includes closer to 40 regions.

I learned from McKee that football players—not rocket scientists—tend to have bigger brains than the average Joe. “It’s because they’re bigger guys,” McKee remarked. But the two brains here were not as big as they should have been. One was 1,120 grams (almost 40 ounces), when it should have been at least 1,350, and another—from a much older, retired player—was just 820 grams. She pointed out obvious defects, where a septum was missing and the amygdala was “almost nonexistent.”

To identify CTE, however, McKee needs to look at stained tissue under a microscope. The buildup of tau within the brain cells is indicative of the disease. She notes that there is a correlation between the parts of the brain afflicted with abnormal tau and the psychological problems of the person before death. McKee finds abnormal tau in the frontal cortex, which is responsible for impulse control, judgment and the ability to multi­task. She also finds it in a deep brain stem structure, the locus coeruleus, which is associated with depression. In later stages, tau is found in the amygdala, which has a role in impulse control, and in the hippocampus, which is important to forming and retaining memories.

After years of denial by the NFL and skepticism within the scientific community, CTE “is now gaining wide acceptance,” McKee says. “We’re definitely past the halfway mark. More and more people are coming around.” Even the NFL has shifted its views, giving the Center for the Study of Traumatic Encephalophathy at Boston University, which McKee co-directs, $1 million for research.

McKee’s more recent findings are an offshoot of this work and are even more controversial. She and her colleagues found that in about 13 percent of CTE cases studied, the deceased had also been diagnosed with ALS—a very high percentage. In the ordinary population, one in about 400 adults is likely to come down with the disease. In autopsies of these cases, McKee found the abnormal tau indicative of CTE but also an exaggerated amount of abnormal TDP-43 proteins, distributed in unusual patterns.

Under a microscope the TDP-43 appears like black lint or flea dust. The protein normally exists in the nucleus of brain cells, but when the cells suffer an axonal injury and become diseased, the proteins come out of the nucleus and build up in the cytoplasm. Abnormal TDP-43 is also found in ALS patients, but Mc­Kee says that in the brains she studied—where the subjects also had CTE—the pattern of TDP-43 distribution is distinct. She found TDP-43 deposits on the surface, around the ventricles and in the brain stem, a pattern atypical of ALS, she says. McKee and her team have given a new name to the disease: chronic traumatic encephalomyelopathy (CTEM).

McKee is clear that her research is far from complete. She does not understand, for instance, the precise role of the tau and TDP-43 proteins in causing the diseases or even if they have a role. “We still don’t really understand it,” she says. “The pathology has established that there is a problem, but it hasn’t answered a lot of questions.” Among them: Why do some people get symptoms of the diseases relatively quickly, whereas others take many years? Why do some people who suffer multiple concussions never have issues? Are some people more genetically susceptible to CTE and CTEM than others? The same or similar questions could apply to smoking and cancer, McKee and her colleagues say. Nobody now questions that smoking causes cancer.

A Leap Too Far?
Many ALS specialists argue that McKee and her co-workers have made broad claims that are not justified by the science. “There is a vast gap in our knowledge,” says Stanley H. Appel, co-director of the Methodist Neurological Institute in Houston. “You don’t know how many concussions it takes, what the risk factors are. You stop suffering concussions, and then, 10 or 15 years later, you have a condition that is devastating? This requires a lot of careful thought and investigation. I’m not critical of careful inquiry. I’m critical when I’m getting panicked calls from a dozen patients who think they may have been misdiagnosed.”

One point Appel and McKee agree on is that ALS is a syndrome, not a single disease. Just as dementia is a big category of diseases, ALS is a category of clinical symptoms. In McKee’s view, CTEM fits under the ALS umbrella—a distinct disorder caused by repetitive concussions. Appel thinks that is a “huge theoretical leap,” unjustified by the published data.

Appel and others suspect that the brains McKee examined with motor neuron degeneration actually had two diseases: CTE and ALS. These critics point out that the strongest scientific studies trying to find a link between concussions and ALS have shown no such connection. “Is it possible that trauma leads to ALS?” Appel asks. “Of course. But top people have been studying that for 30 years and haven’t been able to prove it.”

Ordinary people may not factor in the nuances and fine points of the scientific process when they evaluate their own condition. They are likely to trust their memories—and their personal knowledge of their minds and bodies—to gauge what is happening to them. Kevin Turner and his family and friends feel certain that he has CTE and that he almost surely has CTEM as well. They are somewhat relieved, in a strange way, to have some explanation for what went wrong in Turner’s life.

“I started to play football when I was five years old,” Turner says. “I just really fell in love with the game. From when I was five until I was 31, that’s what I did. I knew that when I got to be 60, I’d have bad knees and a bad back and neck. But nobody talked about the brain. They’d say, ‘Hit with your forehead.’ That was the only way I knew how to do it.”

Turner can remember two times in his professional career when he suffered a severe concussion, once with the Patriots and once with the Eagles. After the second incident, he recalls that he played another quarter but could not remember or figure out what city he was playing in—was it Philadelphia or Green Bay? “But there may have been 100 times when my brain was rattled,” he says. “What is a concussion? What are the criteria? When you hear bells ringing in your head? When you see spots? Or feel dizzy? There were many times, mostly in practice, when all of that happened.”

Dealing With a Death Sentence
By several accounts, Turner was a highly focused, well-organized kid, and that pattern continued into adulthood. “He was good and straight, always on time,” says his University of Alabama roommate and friend, Craig Sanderson, who played wide receiver alongside Turner on the Alabama Crimson Tide. “When we were roommates, he had everything in its place.” But now Sanderson’s living room is evidence of the change that has overcome his friend in recent years. Turner sometimes lives with the Sanderson family, and his belongings—baskets of clothes, blankets, a box of football cards and other personal items—are strewn around the living room. “I’ve seen a distinct personality change,” Sanderson says. “Kevin now has a really hard time taking a task from start to finish.”

Both Sanderson and Turner’s ex-wife, Joyce, say that he has suffered from depression. At first, they thought it was because he was retired from football and dealing with the lifestyle changes involved in returning to the ordinary world. Turner also suffered from a severe addiction to painkillers when he left the game. On top of that, his real estate business went bust. It is not hard to imagine that Turner’s psychological problems—the depression, lack of focus—are connected to those difficulties. But his friends and family say the problems he has encountered are out of character, and now they have another explanation: his personal failures are typical of a significant number of ex-football players who, on autopsy, have a brain gummed up with tau. The behavioral and personality changes “can be considered psychological, but in reality, they’re structural,” McKee says.

“CTE really grabbed my attention because player after player I know had gone through many of the same problems as I had,” says Turner, who has created a foundation to support research into the issue. “I still don’t know that it’s the reason for my troubles, but it’s important to me to think that I’m not alone. At least 14 other guys have gone through similar things: addiction, divorce, bankruptcy. I was just in the special group that got ALS, too. But it gives me a little bit of solace that it wasn’t just me turning into a loser overnight.”

Abnormal tau can be identified only on autopsy, so nothing will be fully clear about Turner’s case until then. He has arranged to donate his brain and spinal cord to McKee’s research group. But he and his family feel confident about what the results will show.

Even so, Turner still loves the game of football. Both his sons play. Nolan is 14, and Cole is eight. (Turner nonetheless held his two sons out of football last autumn. He wants to be able to spend time with the boys while he still has use of his legs, and he wants his youngest son to avoid possible concussions at least until he gets to middle school.) They live with their mother in a modern brick house, with a trampoline and a skateboard ramp in the back driveway. “If they quit football, I’ll be happy, but I have a hard time making them quit,” says Turner, who retains a wry sense of humor about his predicament. “It’s something that’s been a big part of my life, and I can’t just hate it. Just like my ex-wife: I have a hard time hating her.”

Joyce Turner describes herself as angry over the whole sad situation. “He was this happy-go-lucky guy, and then he was depressed,” she says. “He didn’t want anyone to know he was suffering. But he couldn’t make a decision, couldn’t get anything finished. It was like living with a fourth child or like a brother or best friend you’re always angry at. Three years before the ALS diagnosis, he wanted to kill himself. He had some guns. He told me he wanted to kill himself because he just wasn’t himself anymore. But he wouldn’t because of the children.

“I hate what he has gone through, emotionally and physically, because of football. When he got knee injuries, he saw the best surgeons and the best physical therapists. But when he was getting his brains bashed around, he went right back into the game,” she says. “It’s like when we didn’t know that smoking was bad for us.”

Critics say the smoking analogy does not really hold when it comes to CTEM. Carmel Armon, chief of the neurology division at the Baystate Medical Center in Springfield, Mass., and professor of neurology at the Tufts University School of Medicine, believes that the data linking smoking to cancer, going back as far as 1950, are much more solid than the data presented by McKee and her colleagues on concussions and motor neuron disease. That evidence is poor, in Armon’s opinion, and cannot be used to infer any association other than the chance coexistence of two diseases: CTE and ALS.

“There are many nuances that apply to data even when they are clear-cut,” Armon says. For instance, tau and TDP-43 could be causal agents of brain disease, or they could be part of a response mechanism in the brain to fight the disease. Even if they are causal, they could be contributing to two different diseases. “The data don’t support that CTE and CTEM are part of one continuum,” Armon asserts.

Having said that, Armon adds that he has no doubt that concussions are bad for you. “It becomes a social question: Why does society encourage sports in which people are subject to multiple concussions?” he asks. “We used to have gladiators, and now we don’t. No amount of scientific discussion is going to make it healthy to have multiple concussions.”

McKee concurs on that point, but she also believes she can find remedies. Her work is aimed at a better understanding of the ways in which concussions lead to degeneration of the brain and may produce “enormous insight into potential therapeutic interventions,” she says. For people like Kevin Turner and his family, it may be too late. But that is the only hope.