The Boy Who Was Raised as a Dog Read online

  “You can just put those on the table,” Sara said as she walked to the back of the one-room apartment to put the baby down on a mattress against the wall. In two steps I was at the kitchen table. I put the bags down and glanced around the room. There was one couch facing a color television and a small coffee table with a few cups and dirty dishes on it. On a small table with three unmatched chairs near the kitchenette, there was a loaf of Wonderbread and a jar of peanut butter. One double mattress sat on the floor, with blankets and pillows neatly folded at one end. Clothes and newspapers were scattered around. A picture of Martin Luther King Jr. hung on the wall, and next to it on either side were brightly colored school portraits of Tina and her brother. On another wall hung a picture of Sara and the baby, slightly crooked. The apartment was warm.

  Sara stood and awkwardly said, “Thanks again for the ride.” and I assured her it had been no trouble. The moment was very uncomfortable.

  As I walked out the door and said, “See you all next week,” Tina waved. She and her toddler brother were putting the groceries away. They were better behaved than many children I’d seen in much better circumstances; it seemed to me that they had to be.

  The drive home took me through some of the poorest neighborhoods in Chicago. I felt guilty. Guilty about the luck, the opportunities, the resources and the gifts I had been given, guilty about all of the times I had complained about working too much, or not getting credit for something I had done. I also felt I knew much more about Tina. She had grown up in a world so very different from mine. And somehow that had to be related to the problems that brought her to see me. I didn’t know exactly what it was, but I knew there was something important about how the world she grew up and lived in had shaped her emotional, behavioral, social and physical health.

  AFTERWARDS, OF COURSE, I was afraid to tell anyone what I’d done, that I’d driven a patient and her family home. Worse yet, that I had stopped at the store on the way and helped bring in some groceries. But part of me didn’t care. I knew I’d done the right thing. You just don’t let a young mother with two young children and a baby stand in the cold like that.

  I waited two weeks and then, when I next met with Dr. Dyrud, I told him. “I saw them waiting for a bus and it was cold. So I gave them a ride home,” I said nervously, scanning his face for his reaction, just like Tina had done with me. He laughed as I slowly told him about the extent of my transgression.

  When I’d finished, he clapped his hands together, saying, “Great! We should do a home visit with all of our patients.” He smiled and sat back. “Tell me all about it.”

  I was shocked. In an instant Dr. Dyrud’s smile and the delight on his face released me from two weeks of nagging guilt. When he asked what I’d learned I told him that one moment in that tiny apartment had told me more about the challenges facing Tina and her family than I could ever have learned from any on-site session or interview.

  Later in that first year of my child psychiatry fellowship Sara and her family moved to an apartment closer to the medical center, one twenty-minute bus ride away. The lateness ceased. No more “resistance.” We continued to meet once a week.

  DR. DYRUD’S WISDOM and mentorship continued to be liberating for me. Like other teachers, clinicians and researchers who had inspired me, he encouraged exploration, curiosity and reflection, but, most importantly, gave me the courage to challenge existing beliefs. Taking bits and pieces from each of my mentors, I began to develop a therapeutic approach that sought to explain emotional and behavioral problems as symptoms of dysfunction within the brain.

  In 1987 child psychiatry had not yet embraced the neurosciences. In fact, the vast expansion of research on the brain and brain development that began in the 1980s and exploded in the 1990s (“the decade of the brain”) had yet to occur, let alone influence clinical practice. Instead, there was active opposition by many psychologists and psychiatrists to taking a biological perspective on human behavior. Such an approach was considered mechanistic and dehumanizing, as though reducing behavior to biological correlates automatically meant that everything was caused by genes, leaving no room for free will and creativity, and no way to consider environmental factors like poverty. Evolutionary ideas were seen as even worse, as backwards racist and sexist theories that rationalized the status quo and reduced human action to animal drives.

  Since I was just starting out within child psychiatry, I didn’t yet trust my own capacity to think independently, to process and interpret accurately what I was seeing. How could my thoughts about this be right when none of the other established psychiatrists, the stars, my mentors, were talking about or teaching about these things?

  Fortunately, Dr. Dyrud and several of my other mentors encouraged my tendency to fold neuroscience into my clinical thinking about Tina and other patients. What was going on in Tina’s brain? What was different about her brain that made her more impulsive and inattentive than other girls her age? What had happened in her rapidly developing brain when she had suffered these abnormal, sexualized experiences as a toddler? Did the stress of poverty affect her? And why did she have speech and language delays? Dr. Dyrud used to point to his head as he said, “The answer is in there somewhere.”

  My introduction to neuroscience had started during my freshman year in college. My first college advisor, Dr. Seymour Levine, a world-famous neuroendocrinologist, had conducted pioneering work on the impact of stress during early life on the development of the brain, which had shaped all of my subsequent thinking. His work helped me see how early influences can literally leave imprints on the brain that last a lifetime.

  Levine had done a series of experiments examining the development of important stress-related hormone systems in rats. His group’s work demonstrated that the biology and function of these important systems could be altered dramatically by brief periods of stress during early life. Biology isn’t just genes playing out some unalterable script. It is sensitive to the world around it, as evolutionary theories predicted. In some of the experiments the duration of the stress was only minutes long, involving just a few moments of human handling of rat pups (baby rats), which is highly stressful for them. But this very brief stressful experience, at a key time in the development of the brain, resulted in alterations in stress hormone systems that lasted into adulthood.

  From the moment I started my formal education in the field, then, I was aware of the transformative impact of early life experiences. This became a template against which I compared all subsequent concepts.

  Frequently, while at the lab, my thoughts would turn to Tina and the other children with whom I was working. I would force myself to work the problem: What do I know? What information is missing? Can I see any connections between what was known and what was not known? Was seeing me making any difference in the lives of these children? As I thought about my patients, I also considered their symptoms: Why these particular problems in this particular child? What could help change them? Could their behavior be explained by anything that I and other scientists in my field were learning about how the brain works? For example, could studying the neurobiology of attachment—the connection between parent and child—help solve problems between a mother and her son? Could Freudian ideas like transference—where a patient projects his feelings about his parents into other relationships, particularly the one he has with his therapist—be explained by examining the function of the brain?

  There had to be some link, I thought. Just because we couldn’t describe it or yet understand it, there just had to be a correlation between what went on in the brain and every human phenomenon and symptom. After all, the human brain is the organ that mediates all emotion, thought and behavior. In contrast to other specialized organs in the human body, such as the heart, lungs and pancreas, the brain is responsible for thousands of complex functions. When you have a good idea, fall in love, fall down the stairs, gasp when walking up stairs, melt at the smile of your child, laugh at a joke, get hungry and feel full—all of those exp
eriences and all your responses to these experiences are mediated by your brain. So it followed that Tina’s struggles with speech and language, attention, impulsivity, healthy relationships, also had to involve her brain.

  But what part of her brain, and could understanding this help me treat her more effectively? Which of Tina’s brain regions, neural networks, neurotransmitter systems were poorly regulated, underdeveloped or disorganized, and how could this information help me with Tina’s therapy? To answer these questions I had to start with what I already knew.

  THE BRAIN’S REMARKABLE functional capabilities come from an equally remarkable set of structures. There are 100 billion neurons (brain cells), and for each neuron there are ten equally important support cells, called glia. During development—from the first stirrings in the womb to early adulthood—all of these complicated cells (and there are many different types), must be organized into specialized networks. This results in countless intricately interconnected and highly specialized systems. These chains and webs of connected neurons create the varied architecture of the brain.

  For our purposes there are four major parts of the brain: the brainstem, the diencephalon, the limbic system and the cortex. The brain is organized from the inside out, like a house with increasingly complicated additions built on an old foundation. The lower and most central regions of the brainstem and the diencephalon are the simplest. They evolved first, and they develop first as a child grows. As you move upward and outward, things get increasingly more complex with the limbic system. The cortex is more intricate still, the crowning achievement of brain architecture. We share similar organization of our lowest brain regions with creatures as primitive as lizards, while the middle regions are similar to those found in mammals like cats and dogs. The outer areas we share only with other primates, like monkeys and the great apes. The most uniquely human part of the brain is the frontal cortex, but even this shares 96 percent of its organization with that of a chimpanzee!

  Our four brain areas are organized in a hierarchical fashion: bottom to top, inside to outside. A good way to picture it is with a little stack of dollar bills—say five. Fold them in half, place them on your palm and make a hitchhiker’s fist with your thumb pointing out. Now, turn your fist in a “thumbs down” orientation. Your thumb represents the brainstem, the tip of your thumb being where the spinal cord merges into the brainstem; the fatty part of your thumb would be the diencephalon; the folded dollars inside your fist, covered by your fingers and hand, would be the limbic system; and your fingers and hand, which surround the bills, represent the cortex. When you look at the human brain, the limbic system is completely internal; you cannot see it from the outside, just like those dollar bills. Your little finger, which is now oriented to be the top and front, represents the frontal cortex.

  While interconnected, each of these four main areas controls a separate set of functions. The brainstem, for example, mediates our core regulatory functions such as body temperature, heart rate, respiration and blood pressure. The diencephalon and the limbic system handle emotional responses that guide our behavior, like fear, hatred, love and joy. The very top part of the brain, the cortex, regulates the most complex and highly human functions such as speech and language, abstract thinking, planning and deliberate decision making. All of them work in concert, like a symphony orchestra, so while there are individualized capacities, no one system is wholly responsible for the sound of the “music” you actually hear.

  Tina’s symptoms suggested abnormalities in almost all of the parts of her brain. She had sleep and attention problems (brainstem), difficulties with fine motor control and coordination (diencephalon and cortex), clear social and relational delays and deficits (limbic and cortex) and speech and language problems (cortex).

  This pervasive distribution of problems was a very important clue. My research—and the research of hundreds of others—indicated that all of Tina’s problems could be related to one key set of neural systems, the ones involved in helping humans cope with stress and threat. Coincidentally, those were exactly the systems I was studying in the lab.

  These systems were “suspect” to me for two main reasons. The first was that myriad studies in humans and animals had documented the role these systems play in arousal, sleep, attention, appetite, mood, impulse regulation—basically all of the areas in which Tina had major problems. The second reason was that these important networks originate in the lower parts of the brain and send direct connections to all of the other areas of the brain. This architecture allows a unique role for these systems. They are capable of integrating and orchestrating signals and information from all of our senses and throughout the brain. This capacity is necessary to effectively respond to threat: if, for example, a predator may be lurking, an animal needs to be able to respond just as quickly to his scent or sound as to actually seeing him.

  Additionally, the stress-response systems are among only a handful of neural systems in the brain that, if poorly regulated or abnormal, can cause dysfunction in all four of the main brain areas—just like what I was seeing with Tina.

  The basic neuroscience work I’d been doing for years had involved examining the details of how these systems worked. In the brain, neurons transmit messages from one cell to the next by using chemical messengers called neurotransmitters that are released at specialized neuron-to-neuron connections called synapses. These chemical messengers fit only into certain, correctly shaped receptors on the next neuron, in the same way that only the right key will fit into the lock on your front door. Synaptic connections, at once astoundingly complex and yet elegantly simple, create chains of neuron-to-neuron-to-neuron networks that allow all of the many functions of the brain, including thought, feeling, motion, sensation and perception. This also allows drugs to affect us, because most psychoactive medications work like copied keys, fitting into the locks meant to be opened by particular neurotransmitters and fooling the brain into opening or closing their doors.

  I had done my doctoral research in neuropharmacology in the lab of Dr. David U’Prichard, who had trained with Dr. Solomon Snyder, a pioneering neuroscientist and psychiatrist. (Dr. Snyder’s group was famous for, among many other things, finding the receptor at which opiate drugs like heroin and morphine act.) When I worked with Dr. U’Prichard I did research on the norepinephrine (also known as noradrenaline) and epinephrine (also known as adrenaline), systems. These neurotransmitters are involved in stress. The classic “fight or flight” response begins in a central clump of norepinephrine neurons known as the locus coeruleus (“blue spot,” named for its color). These neurons send signals to virtually every other important part of the brain and help it respond to stressful situations.

  Some of my work with Dr. U’Prichard involved two different strains of rats, which are animals of the same species that had some slight genetic differences. These rats looked and acted exactly the same in ordinary situations, but even the most moderate stress would cause one type to break down. Under calm conditions, these rats could learn mazes, but give them the tiniest stress, and they would unravel and forget everything. The other rats were unaffected. When we examined their brains, we found that early in the development of the stress-reactive rats, there was over-activity in their adrenaline and noradrenaline systems. This small change led to a great cascade of abnormalities in receptor number, sensitivity and function across many brain areas, and ultimately altered their ability to respond properly to stress for a lifetime.

  I had no evidence that Tina was genetically “oversensitive” to stress. I did know, however, that the threat and the painful sexual assaults Tina experienced had, no doubt, resulted in repetitive and intense activation of her threat-mediating stress response neural systems. I recalled Levine’s work that had shown that just a few minutes of stressful experience early in life could change a rat’s stress response forever. Tina’s abuse had gone on much longer—she’d been assaulted at least once a week for two years—and that had been compounded by the stress of liv
ing in a constant state of crisis with a family that was often on the economic edge. It occurred to me that if both genes and environment could produce similar dysfunctional symptoms, the effect of a stressful environment on a person already genetically sensitive to stress would probably be magnified.

  And as I continued to work both with Tina and in the lab, I came to believe that in Tina’s case the repeated activation of her stress response systems from a trauma endured at a young age, when her brain was still developing, had probably caused a cascade of altered receptors, sensitivity and dysfunction throughout her brain, similar to the one I observed in animal models. Consequently, I started to think Tina’s symptoms were the result of developmental trauma. Her attention and impulse problems might be due to a change in the organization of her stress response neural networks, a change that might have once helped her cope with her abuse, but was now causing her aggressive behavior and inattention to her class work in school. It made sense: a person with an overactive stress system would pay close attention to the faces of people like teachers and classmates, where threat might lurk, but not to benign things like classroom lessons. A heightened awareness of potential threat might also make someone like Tina prone to fighting, as she would be looking everywhere for signs that someone might be about to attack her again, likely causing her to overreact to the smallest potential signals of aggression. This seemed a much more plausible explanation for Tina’s problems than assuming that her attention problems were coincidental and unrelated to the abuse.

  I looked back through her chart and saw that upon her first visit to the clinic her heart rate had been 112 beats per minute. Normal heart rate for a girl of that age should have been below 100. An elevated heart rate can be an indication of a persistently activated stress response, which was more evidence for my idea that her problems were a direct result of her brain’s response to the abuse. If I had to give Tina a label now, it wouldn’t be ADD, but rather post-traumatic stress disorder, PTSD.