Shrinks (36 page)

Your brain has evolved to help you to survive and enable you to make the best split-second decisions in life-threatening situations. Though your amygdala is screaming at you to run for your life, the most beneficial course of action is to hold your amygdala-stoked emotions in check while you analyze the situation and choose the best option. Perhaps you are more likely to survive if you stand still so that the bear won’t notice you, perhaps you should yell and make loud noises to frighten it or pick up a large stick to defend yourself, or perhaps the smartest option is to pull out your cell phone and call the park rangers. But you will only be able to make a decision if you consciously overcome your emotional urges, a process that neuroscientists call
cognitive control
. Your decision making and cognitive control are handled by the newest and most highly evolved part of your brain, the prefrontal cortex. The more experienced and mature we are, the more likely our prefrontal cortex will be able to exert cognitive control and override our amygdala’s insistent impulse to flee.

But let’s say that you are so scared that your prefrontal cortex can’t counteract your fear. Your amygdala wins out and you start racing for your car as fast as your feet will carry you. The bear spots you and, with a loud growl, gives chase. Fortunately, you outrace the bear, making it to your car and slamming the door just as the bear lunges at you. You’ve survived. Your brain is designed to learn from this valuable life-preserving experience. Your hippocampus now forms a long-term memory of the bear and your decision to flee, a memory that is emotionally saturated with the amygdala’s fear.

The primary reason for the existence of your amygdala–prefrontal cortex–hippocampus system is to enable you to learn from your experiences and improve your ability to react to similar circumstances in the future. The next time you encounter a bear (or a wolf, or a boar, or a cougar) in the woods (or a jungle, or a field), your stored memory will be triggered by the event’s similarity to your original bear encounter and the memory will automatically guide you to react swiftly:
Holy cow, another bear? I survived by running last time, so I better run again!

But what if your original experience fleeing the bear was so traumatic and terrifying that your amygdala lit up like Times Square? Maybe the bear caught up to you before you reached the car and managed to claw your back before you hopped inside. Then it’s possible that your amygdala was firing so wildly it forged a traumatic memory in your hippocampus with searing emotional intensity. Since the stored memory is so powerful, when it is triggered it overwhelms your prefrontal cortex and prevents you from exercising cognitive control. Moreover, in the future the memory might be triggered by stimuli that only vaguely resemble the original event, such that the next time you saw any furry animal—even your neighbor’s poodle—the sight might trigger your original memory, causing your amygdala to instinctively react as if you are again being threatened by a deadly bear—
Holy cow, I better run again!

In other words, individuals afflicted with PTSD cannot separate the details of a new experience from the emotional charge of a past trauma and cannot prevent their amygdala-hippocampus circuit from reliving the mental intensity of the original event. This is what happened to Adrianne Haslet.

On a bright, sunny Patriots’ Day in 2013, Adrianne Haslet stood near the finish line of the Boston marathon, a few yards away from an explosive-laden stainless-steel pressure cooker stuffed in an abandoned backpack. When it exploded, her foot was blown off. The experience would be horrific for anyone—but it was especially traumatic for Adrianne, a dancer who had devoted her life to the nimble use of her feet. Her amygdala maxed out, sending a blistering emotional signal to her hippocampus, which stored a hyperpotent memory of the explosion and its grisly aftermath.

A few months later, after her discharge from Mass General Hospital, Adrianne was back in her Boston apartment when she was suddenly startled by another series of loud explosions—the city’s Fourth of July fireworks display. The sounds of the holiday pyrotechnics ripped through her brain and instantly activated her memory of the marathon explosion, forcing her to relive the same feelings of terror she felt while lying on the blood-drenched sidewalk on Boylston Street. Frantic, she called 911 and begged the helpless dispatcher to halt the fireworks.

Most of us have experienced a milder, nonpathological form of this neural phenomenon during events that are dramatic and unexpected but not quite horrifying. Many people can remember where they were when they heard that President Reagan was shot or learned about the Challenger space shuttle explosion or watched the September 11 attacks unfold. These are sometimes called “flashbulb memories,” and they are the benign non–emotion laden equivalent of the searing, mind-bending memories that PTSD victims can’t get out of their heads.

Using knowledge of the neural mechanism of trauma, recent research has shown that if a person takes a memory-disrupting drug shortly after a traumatic experience—even hours later—PTSD can be drastically reduced, since the hippocampus is prevented from fully consolidating what would become a traumatic memory. (This research was grounded in Eric Kandel’s work demonstrating how short-term memories are encoded into long-term memory.) Research also points to genetic variability in our susceptibility to PTSD. Specific genes involved with the brain mechanisms that control arousal, anxiety, and vigilance seem to be correlated with whether or not a person develops PTSD symptoms. While every person has a breaking point and is capable of developing PTSD if stressed long or hard enough, each person’s breaking point is different.

The dynamics of the amygdala–prefrontal cortex–hippocampus circuit may help explain why I developed my own PTSD-like symptoms after I dropped the air conditioner but not after my home invasion, and why Mr. Kronsky developed intractable symptoms following the death of his son, while Mrs. Kronsky recovered. The crucial factor was cognitive control.

When I was being robbed, my prefrontal cortex enabled me to keep my cool and gave me the sense (however illusory it may have been) that I was in control through the belief that if I made the decision to obey my attackers I would survive unharmed. Since I escaped without serious injury or significant loss, my hippocampus committed to memory an experience that was tempered by my sense of cognitive control. In contrast, once the air conditioner slipped from my fingers, there was absolutely nothing I could do other than shout impotently as it plummeted toward the sidewalk. There was no control, real or illusory, to mitigate my amygdala’s blaring alarm. Thus my hippocampus stored a memory of the experience that was as vivid as a sports arena Jumbotron.

The situation was different with Mr. Kronsky. The fact that he was driving the car would seem to have given him some sense of cognitive as well as physical control over the situation. However, in reality, Kronsky had little influence over the accident’s circumstances in which he was both a passive victim and an observer. Consequently, his hippocampus likely stored a memory that combined the emotional intensity of Edmund’s grisly demise with the guilt-ridden awareness of his role behind the wheel. In this case, his sense of cognitive control became a mental prison, plaguing him with endless “what ifs”: “what if I had not wanted to leave the party early?” “what if I had taken a different route home?” “what if I had driven more slowly through the intersection?”

Since I survived my home invasion unscathed, my own sense of cognitive control helped mitigate the emotional intensity of the experience. But if the two thugs who broke into my apartment had ended up shooting me or stealing my grandfather’s watch, then the same decision to stay calm might have instead thrust me into my own never-ending labyrinth of self-recrimination. Such is the relationship between the brain and our experiences. That which can teach us can also wound us.

Chapter 9

The Triumph of Pluralism: The
DSM-5

Psychiatry is neurology without physical signs, and calls for diagnostic virtuosity of the highest order.

—H
ENRY
G
EORGE
M
ILLER
, B
RITISH
J
OURNAL OF
H
OSPITAL
M
EDICINE
, 1970

I identify humility rather than hubris as the proper basis of scientific maturity. The ideal is not truth or certainty, but a continual and pluralistic pursuit of knowledge.

—H
ASOK
C
HANG

Diagnosis in the Digital Age

The fourth edition of the Bible of Psychiatry was published in 1994. It contained 297 disorders (up from 265) and followed the same framework that Spitzer had laid out in the
DSM-III
. While the publication of the
DSM-III
had been marked by tumult and controversy, the release of the
DSM-IV
was as routine and uneventful as the opening of a Starbucks. Most mental health professionals hardly noticed the process of its construction; they simply began using it when it was released.

The fifth edition, however, was a different story. In 2006, the APA officially authorized the appointment of a new Task Force to develop the
DSM-5
. Much had changed in the world of medicine and psychiatry since the paradigm-shattering
DSM-III
was released in 1980. President George H. W. Bush had proclaimed the 1990s the Decade of the Brain, and neuroscience had burgeoned into one of the most important and dynamic disciplines in the life sciences. Imaging and genetics thoroughly permeated the medical field. There was an abundance of new drugs, new psychotherapy techniques, and new medical devices and technologies.

At the same time, the power and functionality of computers had increased drastically, and the Internet had become a pervasive social force.

In recognition of the new digital era into which the fifth edition would be born, the
Manual
’s abbreviation was changed to
DSM-5
instead of
DSM-V
. By replacing the Roman numeral with a number, the APA suggested that the
DSM
would now be a “living document” and revised iteratively like computer software, and promised the possible release of a
DSM-5.1
and
5.2
.

In 2006, APA president Steve Sharfstein appointed David Kupfer as chair of the Task Force and Darrel Regier as vice chair. Kupfer was the chair of the psychiatry department at the University of Pittsburgh and a world-renowned expert in depression and bipolar disorder. Regier was a psychiatrist and epidemiologist who had cut his teeth on the landmark Epidemiologic Catchment Study, a 1980s NIMH project that measured the rates of mental disorders in the American population.

Kupfer and Regier assembled their team, which went to work in 2007. Like previous
DSM
Task Forces, they conducted extensive literature reviews, analyzed data, and solicited feedback from colleagues and professionals to help them formulate revisions to the existing diagnoses. But unlike previous Task Forces, muffled complaints could soon be heard: There wasn’t a consistent set of procedures for changing diagnoses; there wasn’t a clear plan for assembling the diagnoses into a new edition. In addition, interested parties, both within and outside the profession, observed that the process of reviewing and revising the
DSM
was being orchestrated behind closed doors. Hearing rumblings of discontent, a new generation of antipsychiatry activists, including Robert Whittaker, Gary Greenberg, Peter Breggin, and a reinvigorated Church of Scientology, began to take swipes at the project.

This wasn’t the ’70s, when criticism of the
DSM-III
unfolded almost entirely within the insular world of the mental health profession, with opponents jousting through journal commentaries, typewritten letters, and private meetings. This was the twenty-first century, the age of the Internet and social media. Even nonprofessionals were now empowered to communicate their grievances through blogs, online newsletters, activist websites, Facebook posts, and eventually Twitter. Capturing the spirit of much of the early criticism of the
DSM-5
, Gary Greenberg, a psychotherapist and writer of antipsychiatry screeds, declared in a
New York Times
interview, “No one puts much stock in the actual content of the
DSM
, and even those who defend it acknowledge that its primary virtue is that there isn’t anything else to use.”

The familiar antipsychiatry critics were next joined by voices from stakeholder groups who wanted to know how the
DSM
process would affect their constituencies. Patient advocacy organizations such as the National Alliance for the Mentally Ill, Autism Speaks, the Depression and Bipolar Support Alliance, and the American Foundation for Suicide Prevention also began to complain online that their constituents were being kept in the dark about the formative
DSM-5
process. Soon, there were myriad blogs and online discussions castigating the opaqueness of the
DSM-5
’s development. By failing to respond to this flurry of online salvos, the APA and the
DSM-5
Task Force gave the impression that those in charge were not taking the complaints seriously—or were simply out of touch.