by Ken Dryden
Copyright © 2017 by Ken Dryden
Hardcover edition published 2017
Signal and colophon are registered trademarks of McClelland & Stewart All rights reserved. The use of any part of this publication reproduced, transmitted in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, or stored in a retrieval system, without the prior written consent of the publisher—or, in case of photocopying or other reprographic copying, a licence from the Canadian Copyright Licensing Agency—is an infringement of the copyright law.
Library and Archives Canada Cataloguing in Publication is available upon request.
ISBN: 9780771027475
Ebook ISBN 9780771027482
Library of Congress Control Number is available upon request
Book design by Five Seventeen
Cover image: Steve Montador #4 of the Buffalo Sabres listens to the National Anthem before playing the San Jose Sharks on February 13, 2010 at HSBC Arena in Buffalo, New York. (Photo by Bill Wippert/NHLI via Getty Images)
Published by Signal,
an imprint of McClelland & Stewart,
a division of Penguin Random House Canada Limited,
a Penguin Random House Company
www.penguinrandomhouse.ca
v4.1
a
To Khaya, Hunter, Mara, and Blake,
and tomorrow’s players everywhere
Contents
Cover
Title Page
Copyright
Dedication
Author’s Note
Chapter One
Chapter Two
Chapter Three
Chapter Four
Chapter Five
Chapter Six
Chapter Seven
Chapter Eight
Chapter Nine
Chapter Ten
Chapter Eleven
Chapter Twelve
Chapter Thirteen
Chapter Fourteen
Chapter Fifteen
Chapter Sixteen
Chapter Seventeen
Chapter Eighteen
Chapter Nineteen
Chapter Twenty
Chapter Twenty-One
Chapter Twenty-Two
Chapter Twenty-Three
Acknowledgments
About the Author
AUTHOR’S NOTE
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 play—but 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 Steve’s death, I wanted to know how, and why, a thirty-five-year-old, recently retired hockey player had died.
This is Steve’s story, and it’s the story of a game—of 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 death—as a result of Alzheimer’s perhaps, or Parkinson’s, or amyotrophic lateral sclerosis (ALS), or chronic traumatic encephalopathy (CTE). Hazrati is not a hockey fan and did not know Montador’s 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 country’s 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. Hazrati’s 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 quickly—as 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 son’s brain.
Two weeks later, Steve’s 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 brain’s tissue. Hazrati cut open the bag and put Steve’s brain in a blue hairnet—the kind hospital workers wear—and 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 noted—but then, there rarely is—and 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 hospital’s forty-fifth autopsy case in 2015.
Steve’s brain remained inside the bucket, in a storage area off the autopsy room, for two more weeks, “to fix properly,” as Hazrati puts it—for 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 Steve’s 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 coroner’s 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 cut—from deaths following cardiac surgeries, from general autopsies, from neurodegenerative cases. But on that day in 2015, she had one: Steve’s. She sees so few brains of “young ones,” as she puts it—those 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 Steve’s that looked so normal and healthy—but wasn’t—was a surprise to her. “This was a young person who shouldn’t 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 Steve’s are “very precious,” and extra care must be taken. Not because they are from well-known athletes, but because these athletes have died so young—and 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 haven’t 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 Alzheimer’s, Parkinson’s, ALS, and other neurodegenerative diseases for decades. They still don’t 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 le
ss 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?
Hazrati laid Steve’s brain on the stainless steel table and began to cut. Her knife was long and razor-blade thin, sharp enough to slice through the full width and depth of the brain in one motion without tearing the tissue. Each cutting was about a half centimetre thick, a complete and smooth cross-section that captured all of the brain’s structures and allowed Hazrati to compare one side to the other. She then used a scalpel to cut the tissue into even smaller segments. The hospital’s technicians will embed these segments into wax to protect them and make them easier to handle, then put them into cassettes, and place them into a processor for a few days, in a bath of xylene, chlorine, alcohol, and formalin. Other organs require less time to hydrate and “fix,” but a brain takes longer because of its high lipid or fat content.
For Hazrati, this day was about seeing that the cuts were done properly, and preparing them and ensuring that each was labelled accurately. There was nothing more that she could do at that moment; there was nothing more she could discover.
Several days later, the next stage of cuttings began. The cuts were much finer this time—using a machine not much different than a sausage slicer, only smaller—six microns in depth (about one-quarter the thickness of letter paper), and so thin that colour disappears from the cutting and everything becomes transparent to the naked eye, as if nothing is there. The technicians put the new cuttings into another bath, of water this time, to take the wrinkles out of them, then removed them one at a time with a small painter’s brush, placing each on a glass slide. A stain was applied to give definition to the almost-invisible specimen within, which allowed Hazrati “to see inside all those different cells, individually, one by one” with her microscope.
Depending on what she wants to test for, Hazrati can ask the technicians to apply different stains. The regular stain is pink, and with it she can pick up evidence of Parkinson’s but not of Alzheimer’s; the Alzheimer’s proteins are too similar in colour to the stain, and so blend into the pink. Nor can she see CTE with the regular stain.
With Steve’s brain, Hazrati was looking for abnormal proteins, not knowing what she might find: alpha-synuclein, which is evidence of Parkinson’s; TDP-43, which indicates ALS; beta-amyloid, found in those with Alzheimer’s; and ubiquitin, which is related to multiple diseases. Most particularly she was looking for tau, which is found in sufferers of Alzheimer’s, but also in those with CTE. So, on the slides containing tissues from each section of Steve’s brain, a technician also applied a brown stain. This stain contains an antibody that can “recognize” specific proteins such as tau—and, if tau is present, will “go and sit exactly where the tau is,” as Hazrati puts it. The stain binds to the protein and “tags” it, showing the tau as distinctly brown.
Tau occurs naturally in the brain. Healthy tau allows different parts of the brain to communicate with each other, enabling the brain to function. This communication happens neuron to neuron, through long fibres called axons that connect together like the ends of the buckle on a child’s car-seat harness. Tau is in the axons, and gives them the structural integrity they need to forge this connection. Unhealthy tau causes the axons to lose their structural integrity, breaking the link between neurons, interrupting the communication between the brain’s parts, and diminishing the brain’s ability to function. Unhealthy tau, through a microscope, appears as clumps, like a pile of bricks after a house collapses. This is the signature evidence for CTE.
A technician placed a glass cover slip on top of each of the slides containing the samples from Steve’s brain; the cutting was pressed smooth in between. Each slide was labelled by name and surgical number, and assigned a barcode, then put into trays that were delivered to Hazrati’s office. She was working on a separate case when they arrived, and had other surgicals to get to. She decided to put the trays to one side and to examine them on the weekend.
—
On Saturday, March 21, Hazrati arrived in her office at 7:00 a.m. “What you hope for the day you examine your trays is that you’re completely there,” Hazrati says. That you are focused, in other words. “Because you can easily make mistakes. There’s nothing that will jump out at you and tell you that it’s there. It’s up to you to see it. To recognize patterns. It’s what our eyes have been trained to do.” And if she does make mistakes—if she doesn’t see what is there, or if she sees what isn’t—it can misdirect her thinking and set her back weeks. It can affect the next researcher, too, in another case who is also working hard to solve the brain’s puzzle, and the ones after that. Most of all, it can affect some future patient whose hope is in her hands.
Hazrati had other trays to examine that day, but she began with Steve’s. And while most times she starts with her pink-stained slides and goes through all of them before moving on to the brown, this time she started with the brown slides. “I knew this was a young, healthy person and I’m not expecting to see unexpected things,” she says. “So I went right to what nails the question: is tau there or not?” She began with a slide from the frontal lobe. If tau was present, it would show up here.
Divided into two hemispheres, the frontal lobe extends over the top of the head from the crown to the forehead and almost to each ear. In terms of the brain’s function, this is where everything comes together. All of the sensory inputs gathered elsewhere in the brain come to the frontal lobe to be processed, and made sense of, and given meaning. This is where information gets stored in short-term memory, where it is examined and manipulated, where its problems are solved, where its complications are subjected to judgment, where emotions are added, where decisions get made. It is in the frontal lobe where our humanity resides—what makes humans humans. It is where our personality lies—what makes us us.
The temporal lobe begins where the frontal lobe ends, and extends on each side of the brain from the core of the eye to the back of the ear. It is the site of long-term memory. The parietal lobe covers the upper rear quadrant of the brain. It is a place of recognition and understanding—of a face, of language, of space and our orientation to it.
Hazrati had made cuts from each of these parts of the brain, and she examined every slide for anything that the stains might reveal. In Steve’s case, the presence or absence of tau was the answer. But for Hazrati as a researcher, its presence or absence meant a different set of questions. If Steve didn’t have tau, why not? Others with a similar history of concussions had it, so what was different about him? Genetics? The seriousness or frequency of the blows to his head? Or something else? Or maybe it would mean that she had missed something. Maybe something other than tau had caused his symptoms. And if tau were present, the questions would be the same, only reversed.
Hazrati knew that if Steve’s brain showed signs of CTE, that was “amazing.” If it didn’t, it would be amazing for other reasons. In either event, she would be able to add these slides and the remaining block of Steve’s brain tissue to those from every other brain she had worked on, to examine again later if some new brain revealed something that got her thinking in a new way. The answer, as she says, is in the organs. It is where all the information she needs to know lies. It is why Hazrati keeps looking through the eyepiece of her microscope, no matter what she finds—or does not find.
On that Saturday morning, Hazrati sat down at her microscope and pulled out her first slide, which contained matter taken from the frontal lobe. She put it on the glass, and through her eyepiece she was able to see inside the cell, into the neurons, the astrocytes. Later, she looked at slides from the temporal and parietal lobes. What she found gave her a “fuzzy feeling,” as she puts it. She saw the brown that revealed tau.
Steve had CTE.
CHAPTER TWO
Training camp, September 2003. The Calgary Flames had missed t
he playoffs for seven straight years, and had finished the previous season seventeen points behind Edmonton, no less, for the last playoff spot in the Western Conference. With the low value of the Canadian dollar, no NHL salary cap, and a few thousand empty seats at most home games, Calgary, a city known for its optimism, was very pessimistic about the present and the future of the Flames. However, there was some promise. The year before, Darryl Sutter—one of the gritty, no-nonsense Sutters of Viking, Alberta—had been made coach midseason, and with him behind the bench the team had managed a slightly better than .500 record. There were also some young defencemen who were just emerging into their ready-to-contribute years—Robyn Regehr, Jordan Leopold, Toni Lydman, Denis Gauthier, Andrew Ference—and two others, less experienced, who were ready to push them—Mike Commodore and Steve Montador. Steve was twenty-three.
That summer, the Flames had also acquired Rhett Warrener, a defenceman from Buffalo to bring some added stability to the team. Warrener was twenty-seven, and had already played nearly 500 NHL games. “I vividly remember meeting Monty for the first time,” Warrener says. On a team, names quickly become nicknames, and Steve, all his hockey life, had been “Monty.”
“We had just done our first day of physicals at training camp. It was about six o’clock and I was in the restaurant of the Melrose Bar eating dry ribs. I remember that because I’d been living in the U.S. and you can’t get dry ribs in the States. I was the only veteran there. The others were training camp guys trying to make the team. There were about six or seven of us. Monty and I were sitting next to each other. We seemed to laugh at the same jokes. Right away, we seemed to know what the other was thinking. We picked up on each other’s moods. I remember at the end of the night thinking that this guy is going to be a friend. Then, I thought, it’s too bad he’s not going to make the team.”
