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
REEDUCATING THE EMOTIONAL BRAIN
One of the more encouraging findings about PTSD came from a study of Holocaust survivors, about three quarters of whom were found to have active PTSD symptoms even a half century later. The positive finding was that a quarter of the survivors who once had been troubled by such symptoms no longer had them; somehow the natural events of their lives had counteracted the problem. Those who still had the symptoms showed evidence of the catecholamine-related brain changes typical of PTSD—but those who had recovered had no such changes.16 This finding, and others like it, hold out the promise that the brain changes in PTSD are not indelible, and that people can recover from even the most dire emotional imprinting—in short, that the emotional circuitry can be reeducated. The good news, then, is that traumas as profound as those causing PTSD can heal, and that the route to such healing is through relearning.