I never met Steve Montador. In his early seasons with the Calgary Flames, I was president of the Toronto Maple Leafs, so I must have seen him playbut I have no recollection of him.
I love sports. I played sports all my life. My son and daughter played hockey. My two grandsons play today. When I heard the news of Steves death, I wanted to know how, and why, a thirty-five-year-old, recently retired hockey player had died.
This is Steves story, and its the story of a gameof where it began, how it got to be where it is, where it can go from here, and how it can get there.
CHAPTER ONE
It was the morning of February 15, 2015, and Dr. Lili-Naz Hazrati, a neuropathologist at the University Health Network in Toronto, was listening to her radio when she heard the news that Steve Montador, a former NHL defenceman, had died. Hazrati studies the brains of people who have exhibited symptoms of brain disease or dysfunction in the months or years before their deathas a result of Alzheimers perhaps, or Parkinsons, or amyotrophic lateral sclerosis (ALS), or chronic traumatic encephalopathy (CTE). Hazrati is not a hockey fan and did not know Montadors name. But as part of her work, she did know that in recent years CTE has been found in the postmortem examinations of several former football and hockey players.
Born in Iran, Hazrati left with her parents and sister in the midst of the countrys 1979 revolution, settling in Barcelona first, before coming to Canada when she was eighteen. After her first year in university during a summer job in a neurobiology research lab in Quebec City, she learned how to do experiments and surgical procedures, an experience that would set her on her career path. Hazratis interest is the brain, and she is now also a member of a sports concussion research group led by the renowned Toronto neurosurgeon Dr. Charles Tator.
To gather the necessary data for her research, Hazrati needs brains to study. So when she heard about Steve, she knew she had to act quicklyas his was a sudden and unexpected death, there would be an autopsy performed within twenty-four hours. Hazrati called the chief coroner and asked him if he would retain the brain, pending her request to the Montador family for their consent to the donation of their sons brain.
Two weeks later, Steves brain arrived at her office at the Toronto General Hospital (TGH). It was in a cardboard box inside a plastic bag containing a formaldehyde solution called formalin, which helps to preserve the brains tissue. Hazrati cut open the bag and put Steves brain in a blue hairnetthe kind hospital workers wearand placed it in a large white plastic bucket filled with fresh formalin. She then attached the ends of the hairnet to the sides of the bucket, to allow the brain to float in the solution. There was no outward sign of injury or disease, she notedbut then, there rarely isand any difference in weight or configuration since the time of death would be slight. She did not examine the brain further. She labelled the bucket A1545; this was the hospitals forty-fifth autopsy case in 2015.
Steves brain remained inside the bucket, in a storage area off the autopsy room, for two more weeks, to fix properly, as Hazrati puts itfor it to become firm enough to hold its shape for examination and to be cut easily. After those two weeks, Hazrati opened the bucket containing Steves brain and began her examination.
When Hazrati had first seen the brain, it was almost white, with spidery, pinkish-red blood vessels running along its surface. Now the brain was a grey-white colour, with those pinkish-red lines turned red-brown because of the formalin, and its contours more obvious. Hazrati weighed the brain and checked her reading against the one in the coroners report: 1,600 grams (about 3.5 pounds), an increase of ten per cent. This was to be expected, because of the formalin that the brain had absorbed. Again, nothing was unusual.
On a normal day, Hazrati might have three or four brains to cutfrom deaths following cardiac surgeries, from general autopsies, from neurodegenerative cases. But on that day in 2015, she had one: Steves. She sees so few brains of young ones, as she puts itthose who are forty years old or younger, but who during their lifetimes exhibited symptoms of those much older: memory loss, loss of emotional control, loss of cognitive function. Hazrati is rarely shocked by what she sees, because she never anticipates what she will find. She is a scientist, and she must see only what is there. The organ is what gives you the most information, she says. You must let it tell the story. Still, a young brain like Steves that looked so normal and healthybut wasntwas a surprise to her. This was a young person who shouldnt be dead now, she says. His brain should not have been on the autopsy table in front of her, in that small, spare, surgically clean room.
As Hazrati puts it, brains like Steves are very precious, and extra care must be taken. Not because they are from well-known athletes, but because these athletes have died so youngand because the disease these brains contain is so little understood that every glimpse into them matters. They are precious because, for researchers to discover what they havent yet been able to, they need lots of brains in order to gauge differences, uncover similarities, and have new things to think about and new findings to share with other scientists. Researchers have examined brains affected by Alzheimers, Parkinsons, ALS, and other neurodegenerative diseases for decades. They still dont know the causes of these diseases, or how to cure them, but they have studied them enough to know there is a certain predictability to them. This is less so the case with CTE. It seems that the disease is related to blows to the head, but not limited to them. After all, even the most physically inactive among us have hit our heads hard many times in our lives. What is it about the brains of these athletes that are different?