Trauma and Emotional Relearning
Som Chit, a Cambodian refugee, balked when her three sons asked her to buy them toy AK-47 machine guns. Her sons—ages six, nine, and eleven—wanted the toy guns to play the game some of the kids at their school called Purdy. In the game, Purdy, the villain, uses a submachine gun to massacre a group of children, then turns it on himself. Sometimes, though, the children have it end differently: it is they who kill Purdy.
Purdy was the macabre reenactment by some of the survivors of the catastrophic events of February 17, 1989, at Cleveland Elementary School in Stockton, California. There, during the school's late-morning recess for first, second, and third graders, Patrick Purdy—who had himself attended those grades at Cleveland Elementary some twenty years earlier—stood at the playground's edge and fired wave after wave of 7.22 mm bullets at the hundreds of children at play. For seven minutes Purdy sprayed bullets toward the playground, then put a pistol to his head and shot himself. When the police arrived they found five children dying, twenty-nine wounded.
In ensuing months, the Purdy game spontaneously appeared in the play of boys and girls at Cleveland Elementary, one of many signs that those seven minutes and their aftermath were seared into the children's memory. When I visited the school, just a short bike ride from the neighborhood near the University of the Pacific where I myself had grown up, it was five months after Purdy had turned that recess into a nightmare. His presence was still palpable, even though the most horrific of the grisly remnants of the shooting—swarms of bullet holes, pools of blood, bits of flesh, skin, and scalp—were gone by the morning after the shooting, washed away and painted over.
By then the deepest scars at Cleveland Elementary were not to the building but to the psyches of the children and staff there, who were trying to carry on with life as usual.1 Perhaps most striking was how the memory of those few minutes was revived again and again by any small detail that was similar in the least. A teacher told me, for example, that a wave of fright swept through the school with the announcement that St. Patrick's Day was coming; a number of the children somehow got the idea that the day was to honor the killer, Patrick Purdy.
"Whenever we hear an ambulance on its way to the rest home down the street, everything halts," another teacher told me. "The kids all listen to see if it will stop here or go on." For several weeks many children were terrified of the mirrors in the restrooms; a rumor swept the school that "Bloody Virgin Mary," some kind of fantasied monster, lurked there. Weeks after the shooting a frantic girl came running up to the school's principal, Pat Busher, yelling, "I hear shots! I hear shots!" The sound was from the swinging chain on a tetherball pole.
|
|
|
Many children became hypervigilant, as though continually on guard against a repetition of the terror; some boys and girls would hover at recess next to the classroom doors, not daring to venture out to the playground where the killings had occurred. Others would only play in small groups, posting a designated child as lookout. Many continued for months to avoid the "evil" areas, where children had died.
The memories lived on, too, as disturbing dreams, intruding into the children's unguarded minds as they slept. Apart from nightmares repeating the shooting itself in some way, children were flooded with anxiety dreams that left them apprehensive that they too would die soon. Some children tried to sleep with their eyes open so they wouldn't dream.
All of these reactions are well known to psychiatrists as among the key symptoms of post-traumatic stress disorder, or PTSD. At the core of such trauma, says Dr. Spencer Eth, a child psychiatrist who specializes in PTSD in children, is "the intrusive memory of the central violent action: the final blow with a fist, the plunge of a knife, the blast of a shotgun. The memories are intense perceptual experiences—the sight, sound, and smell of gunfire; the screams or sudden silence of the victim; the splash of blood; the police sirens."
These vivid, terrifying moments, neuroscientists now say, become memories emblazoned in the emotional circuitry. The symptoms are, in effect, signs of an overaroused amygdala impelling the vivid memories of a traumatic moment to continue to intrude on awareness. As such, the traumatic memories become mental hair triggers, ready to sound an alarm at the least hint that the dread moment is about to happen once again. This hair-trigger phenomenon is a hallmark of emotional trauma of all kinds, including suffering repeated physical abuse in childhood.
|
|
|
Any traumatizing event can implant such trigger memories in the amygdala: a fire or an auto accident, being in a natural catastrophe such as an earthquake or a hurricane, being raped or mugged. Hundreds of thousands of people each year endure such disasters, and many or most come away with the kind of emotional wounding that leaves its imprint on the brain.
Violent acts are more pernicious than natural catastrophes such as a hurricane because, unlike victims of a natural disaster, victims of violence feel themselves to have been intentionally selected as the target of malevolence. That fact shatters assumptions about the trustworthiness of people and the safety of the interpersonal world, an assumption natural catastrophes leave untouched. Within an instant, the social world becomes a dangerous place, one in which people are potential threats to your safety.
Human cruelties stamp their victims' memories with a template that regards with fear anything vaguely similar to the assault itself. A man who was struck on the back of his head, never seeing his attacker, was so frightened afterward that he would try to walk down the street directly in front of an old lady to feel safe from being hit on the head again.2 A woman who was mugged by a man who got on an elevator with her and forced her out at knife point to an unoccupied floor was fearful for weeks of going into not just elevators, but also the subway or any other enclosed space where she might feel trapped; she ran from her bank when she saw a man put his hand in his jacket as the mugger had done.
The imprint of horror in memory—and the resulting hypervigilance—can last a lifetime, as a study of Holocaust survivors found. Close to fifty years after they had endured semistarvation, the slaughter of their loved ones, and constant terror in Nazi death camps, the haunting memories were still alive. A third said they felt generally fearful. Nearly three quarters said they still became anxious at reminders of the Nazi persecution, such as the sight of a uniform, a knock at the door, dogs barking, or smoke rising from a chimney. About 60 percent said they thought about the Holocaust almost daily, even after a half century; of those with active symptoms, as many as eight in ten still suffered from repeated nightmares. As one survivor said, "If you've been through Auschwitz and you don't have nightmares, then you're not normal."
|
|
|
HORROR FROZEN IN MEMORY
The words of a forty-eight-year-old Vietnam vet, some twenty-four years after enduring a horrifying moment in a faraway land:
I can't get the memories out of my mind! The images come flooding back in vivid detail, triggered by the most inconsequential things, like a door slamming, the sight of an Oriental woman, the touch of a bamboo mat, or the smell of stir-fried pork. Last night I went to bed, was having a good sleep for a change. Then in the early morning a storm front passed through and there was a bolt of crackling thunder. I awoke instantly, frozen in fear. I am right back in Vietnam, in the middle of the monsoon season at my guard post. I am sure I'll get hit in the next volley and convinced I will die. My hands are freezing, yet sweat pours from my entire body. I feel each hair on the back of my neck standing on end. I can't catch my breath and my heart is pounding. I smell a damp sulfur smell. Suddenly I see what's left of my buddy Troy . . . on a bamboo platter, sent back to our camp by the Vietcong.... The next bolt of lightning and clap of thunder makes me jump so much that I fall to the floor.3
This horrible memory, vividly fresh and detailed though more than two decades old, still holds the power to induce the same fear in this ex-soldier that he felt on that fateful day. PTSD represents a perilous lowering of the neural setpoint for alarm, leaving the person to react to life's ordinary moments as though they were emergencies. The hijacking circuit discussed in Chapter 2 seems critical in leaving such a powerful brand on memory: the more brutal, shocking, and horrendous the events that trigger the amygdala hijacking, the more indelible the memory. The neural basis for these memories appears to be a sweeping alteration in the chemistry of the brain set in motion by a single instance of overwhelming terror.4 While the PTSD findings are typically based on the impact of a single episode, similar results can come from cruelties inflicted over a period of years, as is the case with children who are sexually, physically, or emotionally abused.
|
|
|
The most detailed work on these brain changes is being done at the National Center for Post-Traumatic Stress Disorder, a network of research sites based at Veterans' Administration hospitals where there are large pools of those who suffer from PTSD among the veterans of Vietnam and other wars. It is from studies on vets such as these that most of our knowledge of PTSD has come. But these insights apply as well to children who have suffered severe emotional trauma, such as those at Cleveland Elementary.
"Victims of a devastating trauma may never be the same biologically," Dr. Dennis Charney told me.5 A Yale psychiatrist, Charney is director of clinical neuroscience at the National Center. "It does not matter if it was the incessant terror of combat, torture, or repeated abuse in childhood, or a one-time experience, like being trapped in a hurricane or nearly dying in an auto accident. All uncontrollable stress can have the same biological impact."
The operative word is uncontrollable. If people feel there is something they can do in a catastrophic situation, some control they can exert, no matter how minor, they fare far better emotionally than do those who feel utterly helpless. The element of helplessness is what makes a given event subjectively overwhelming. As Dr. John Krystal, director of the center's Laboratory of Clinical Psychopharmacology, told me, "Say someone being attacked with a knife knows how to defend himself and takes action, while another person in the same predicament thinks, I'm dead.' The helpless person is the one more susceptible to PTSD afterward. It's the feeling that your life is in danger and there's nothing you can do to escape it —that's the moment the brain change begins."
Helplessness as the wild card in triggering PTSD has been shown in dozens of studies on pairs of laboratory rats, each in a different cage, each being given mild—but, to a rat, very stressful—electric shocks of identical severity. Only one rat has a lever in its cage; when the rat pushes the lever, the shock stops for both cages. Over days and weeks, both rats get precisely the same amount of shock. But the rat with the power to turn the shocks off comes through without lasting signs of stress. It is only in the helpless one of the pair that the stress-induced brain changes occur.6 For a child being shot at on a playground, seeing his playmates bleeding and dying—or for a teacher there, unable to stop the carnage—that helplessness must have been palpable.
PTSD AS A LIMBIC DISORDER
It had been months since a huge earthquake shook her out of bed and sent her yelling in panic through the darkened house to find her four-year-old son. They huddled for hours in the Los Angeles night cold under a protective doorway, pinned there without food, water, or light while wave after wave of aftershocks tumbled the ground beneath them. Now, months later, she had largely recovered from the ready panic that gripped her for the first few days afterward, when a door slamming could start her shivering with fear. The one lingering symptom was her inability to sleep, a problem that struck only on those nights her husband was away—as he had been the night of the quake.
The main symptoms of such learned fearfulness—including the most intense kind, PTSD—can be accounted for by changes in the limbic circuitry focusing on the amygdala.7 Some of the key changes are in the locus ceruleus, a structure that regulates the brain's secretion of two substances called catecholamines: adrenaline and noradrenaline. These neurochemicals mobilize the body for an emergency; the same catecholamine surge stamps memories with special strength. In PTSD this system becomes hyperreactive, secreting extra-large doses of these brain chemicals in response to situations that hold little or no threat but somehow are reminders of the original trauma, like the children at Cleveland Elementary School who panicked when they heard an ambulance siren similar to those they had heard at their school after the shooting.
The locus ceruleus and the amygdala are closely linked, along with other limbic structures such as the hippocampus and hypothalamus; the circuitry for the catecholamines extends into the cortex. Changes in these circuits are thought to underlie PTSD symptoms, which include anxiety, fear, hypervigilance, being easily upset and aroused, readiness for fight or flight, and the indelible encoding of intense emotional memories.8 Vietnam vets with PTSD, one study found, had 40 percent fewer catecholamine-stopping receptors than did men without the symptoms—suggesting that their brains had undergone a lasting change, with their catecholamine secretion poorly controlled.9
Other changes occur in the circuit linking the limbic brain with the pituitary gland, which regulates release of CRF, the main stress hormone the body secretes to mobilize the emergency fight-or-flight response. The changes lead this hormone to be oversecreted—particularly in the amygdala, hippocampus, and locus ceruleus—alerting the body for an emergency that is not there in reality.10
As Dr. Charles Nemeroff, a Duke University psychiatrist, told me, "Too much CRF makes you overreact. For example, if you're a Vietnam vet with PTSD and a car backfires at the mall parking lot, it is the triggering of CRF that floods you with the same feelings as in the original trauma: you start sweating, you're scared, you have chills and the shakes, you may have flashbacks. In people who hypersecrete CRF, the startle response is overactive. For example, if you sneak up behind most people and suddenly clap your hands, you'll see a startled jump the first time, but not by the third or fourth repetition. But people with too much CRF don't habituate: they'll respond as much to the fourth clap as to the first."11
A third set of changes occurs in the brain's opioid system, which secretes endorphins to blunt the feeling of pain. It also becomes hyperactive. This neural circuit again involves the amygdala, this time in concert with a region in the cerebral cortex. The opioids are brain chemicals that are powerful numbing agents, like opium and other narcotics that are chemical cousins. When experiencing high levels of opioids ("the brain's own morphine"), people have a heightened tolerance for pain—an effect that has been noted by battlefield surgeons, who found severely wounded soldiers needed lower doses of narcotics to handle their pain than did civilians with far less serious injuries.
Something similar seems to occur in PTSD.12 Endorphin changes add a new dimension to the neural mix triggered by reexposure to trauma: a numbing of certain feelings. This appears to explain a set of "negative" psychological symptoms long noted in PTSD: anhedonia (the inability to feel pleasure) and a general emotional numbness, a sense of being cut off from life or from concern about others' feelings. Those close to such people may experience this indifference as a lack of empathy. Another possible effect may be dissociation, including the inability to remember crucial minutes, hours, or even days of the traumatic event.
The neural changes of PTSD also seem to make a person more susceptible to further traumatizing. A number of studies with animals have found that when they were exposed even to mild stress when young, they were far more vulnerable than unstressed animals to trauma-induced brain changes later in life (suggesting the urgent need to treat children with PTSD). This seems a reason that, exposed to the same catastrophe, one person goes on to develop PTSD and another does not: the amygdala is primed to find danger, and when life presents it once again with real danger, its alarm rises to a higher pitch.
All these neural changes offer short-term advantages for dealing with the grim and dire emergencies that prompt them. Under duress, it is adaptive to be highly vigilant, aroused, ready for anything, impervious to pain, the body primed for sustained physical demands, and—for the moment—indifferent to what might otherwise be intensely disturbing events. These short-term advantages, however, become lasting problems when the brain changes so that they become predispositions, like a car stuck in perpetual high gear. When the amygdala and its connected brain regions take on a new setpoint during a moment of intense trauma, this change in excitability—this heightened readiness to trigger a neural hijacking—means all of life is on the verge of becoming an emergency, and even an innocent moment is susceptible to an explosion of fear run amok.
EMOTIONAL RELEARNING
Such traumatic memories seem to remain as fixtures in brain function because they interfere with subsequent learning—specifically, with relearning a more normal response to those traumatizing events. In acquired fear such as PTSD, the mechanisms of learning and memory have gone awry; again, it is the amygdala that is key among the brain regions involved. But in overcoming the learned fear, the neocortex is critical.
Fear conditioning is the name psychologists use for the process whereby something that is not in the least threatening becomes dreaded as it is associated in someone's mind with something frightening. When such frights are induced in laboratory animals, Charney notes, the fears can last for years.13 The key region of the brain that learns, retains, and acts on this fearful response is the circuit between the thalamus, amygdala, and prefrontal lobe—the pathway of neural hijacking.
Ordinarily, when someone learns to be frightened by something through fear conditioning, the fear subsides with time. This seems to happen through a natural relearning, as the feared object is encountered again in the absence of anything truly scary. Thus a child who acquires a fear of dogs because of being chased by a snarling German shepherd gradually and naturally loses that fear if, say, she moves next door to someone who owns a friendly shepherd, and spends time playing with the dog.
In PTSD spontaneous relearning fails to occur. Charney proposes that this may be due to the brain changes of PTSD, which are so strong that, in effect, the amygdala hijacking occurs every time something even vaguely reminiscent of the original trauma comes along, strengthening the fear pathway. This means that there is never a time when what is feared is paired with a feeling of calm—the amygdala never relearns a more mild reaction. "Extinction" of the fear, he observes, "appears to involve an active learning process," which is itself impaired in people with PTSD, "leading to the abnormal persistence of emotional memories."14
But given the right experiences, even PTSD can lift; strong emotional memories, and the patterns of thought and reaction that they trigger, can change with time. This relearning, Charney proposes, is cortical. The original fear ingrained in the amygdala does not go away completely; rather, the prefrontal cortex actively suppresses the amygdala's command to the rest of the brain to respond with fear.
"The question is, how quickly do you let go of learned fear?" asks Richard Davidson, the University of Wisconsin psychologist who discovered the role of the left prefrontal cortex as a damper on distress. In a laboratory experiment in which people first learned an aversion to a loud noise—a paradigm for learned fear, and a lower-key parallel of PTSD—Davidson found that people who had more activity in the left prefrontal cortex got over the acquired fear more quickly, again suggesting a cortical role in letting go of learned distress.15
Дата добавления: 2018-02-28; просмотров: 385; Мы поможем в написании вашей работы! |
Мы поможем в написании ваших работ!