情商：为什么情商比智商更重要（第2版）

幸运的是，我们当中的大多数人很少会遭受大灾大难，从而留下刻骨铭心的创伤记忆。但是在生活比较平静的时刻，也有可能出现创伤记忆肆意影响同一神经回路的现象。童年期常见的煎熬，比如长期受到忽视、得不到父母的关注或关怀、被遗弃、受到排挤等，也许不会上升到创伤的高度，但这些痛苦的记忆肯定会给儿童的情绪脑打下烙印，导致他们将来亲密的人际关系出现扭曲，充满泪水和愤怒。如果说创伤后应激障碍可以得到治疗，那么很多人默默承受的情绪伤痕也可以修复——这就是精神疗法的使命。一般来说，只有通过学习，才能对难以承受的生活压力应付自如，情绪智力才能发挥作用。

前额叶皮层可以根据更全面的信息进行反应。杏仁核与前额叶皮层之间的动态关系为精神疗法重新塑造不良的情绪模式提供了神经解剖学的模型。神经学专家约瑟夫·勒杜克斯发现杏仁核对情绪爆发具有触发器的作用，他指出：“一旦你的情绪系统学会了某种东西，你就可能永远也摆脱不了它。精神疗法的作用是教你怎样加以控制，教会你的新皮层如何抑制你的杏仁核。尽管行动的冲动受到了压制，但你对这种东西的基本情绪还是以受抑的形式潜伏了下来。”

既然大脑结构是情绪再学习的基础，那么即使在精神疗法成功之后，余留的反应，即起源于困扰情绪模式的初始敏感或恐惧感的遗迹，也可能保留下来。^[21]前额叶皮层可以改进或遏制杏仁核狂暴的冲动，但不能在第一时间阻止杏仁核的反应。虽然我们不能决定我们什么时候会情绪爆发，但我们可以较好地控制情绪爆发的持续时间。迅速地从情绪爆发当中复原可以说是情绪成熟的标志。

在精神疗法期间，主要的变化在于一旦触发情绪反应，人们所做出的回应。不过，最初被触发的反应趋势并没有完全消失。雷斯特·柏斯基及其同事进行的一系列关于精神疗法的研究为此提供了证据。^[22]他们分析了几十位接受精神疗法病人的主要人际冲突，比如极度渴望被人接受或寻求亲密关系，或者害怕失败与过度依赖等问题。他们仔细分析了病人在人际关系方面的意愿和恐惧被激活时所做出的典型（总是适得其反）

回应，比如要求过高导致他人愤怒或冷漠无情，或者欲迎还拒，反而弄巧成拙，让别人因为误解而生气。在注定产生恶劣影响的人际交往中，病人充满了不安的情绪——绝望和悲伤，怨恨和愤怒，焦虑和恐惧，内疚和自责等。不管病人的具体表现是什么，这种情况会出现在他们所有重要的人际关系中，无论是和配偶或恋人，孩子或父母，还是同事或上司之间的关系。

在长期治疗过程中，这些病人发生了两种变化：他们对刺激事件的情绪反应不再那么困扰，甚至变得平静或茫然，与此同时，他们的公开回应更有效果，他们获得了真正想从人际关系中得到的东西。不过病人根本的意愿或恐惧以及最初的情感痛苦并没有改变。到精神疗法接近尾声时，病人表示，与刚刚开始接受治疗时相比，他们在人际交往中负面的情绪反应只有原来的一半，而他们从他人身上获得的积极回应是原来的两倍。但是病人基于这些需求的特定感觉完全没有改变。

就大脑而言，面对恐怖事件的种种迹象，边缘神经回路作为回应会拉响警报，不过前额叶皮层和关联区域可以学会更有益的新型回应方式。简而言之，情绪经验——即使是童年期最刻骨铭心的心理习惯，也可以重新塑造。情绪学习是一生的课程。

1. I wrote about the lasting trauma of the killings at Cleveland Elementary School in The New YorkTimes “Education Life” section (Jan. 7, 1990).
2. The examples of PTSD in crime victims were offered by Dr. Shelly Niederbach, a psychologist atthe Victims’ Counseling Service, Brooklyn.
3. The Vietnam memory is from M. Davis, “Analysis of Aversive Memories Using the Fear-Potentiated Startle Paradigm,” in N. Butters and L. R Squire, eds., The Neuro-psychology of Memory(New York: Guilford Press, 1992).
4. LeDoux makes the scientific case for these memories being especially enduring in “Indelibility ofSubcortical Emotional Memories,”J ournal of Cognitive Neuroscience (1989), vol. 1, 238-43.
5. I interviewed Dr. Charney in T he New York Times (June 12, 1990).
6. The experiments with paired laboratory animals were described to me by Dr.John Krystal, and havebeen repeated at several scientific laboratories. The major studies were done by Dr. Jay Weiss at DukeUniversity.
7. The best account of the brain changes underlying PTSD, and the role of the amygdala in them, is inDennis Charney et al., “Psychobiologic Mechanisms of Posttraumatic Stress Disorder,” Archives ofGeneral Psychiatry 50 (April 1993),294-305.
8. Some of the evidence for trauma-induced changes in this brain network comes from experiments inwhich Vietnam vets with PTSD were injected with yohimbine, a drug used on the tips of arrows bySouth American Indians to render their prey helpless. In tiny doses yohimbine blocks the action of aspecificreceptor (the point on a neuron that receives a neurotransmitter) that ordinarily acts as a brakeon the catecholamines. Yohimbine takes the brakes off, keeping these receptors from sensing thesecretion of catecholamines; the result is increasing catecholamine levels. With the neural brakes onanxiety disarmed by the drug injections, the yohimbine triggered panic in 9 of 15 PTSD patients,andlifelike flashbacks in 6. One vet had a hallucination of a helicopter being shot down in a trail of smokeand a bright flash; another saw the explosion by a land mine of a Jeep with his buddies in it—the samescene that had haunted his nightmares and appeared as flashbacks for more than 20 years. Theyohimbine study was conducted by Dr. John Krystal, director of the Laboratory of ClinicalPsychopharmacology at the National Center for PTSD at the West Haven, Conn.,VA Hospital.
9. Fewer alpha-2 receptors in men with PTSD: see Charney, “Psychobiologic Mechanisms.”
10. The brain, trying to lower the rate of CRF secretion, compensates by decreasing the number ofreceptors that release it. One telltale sign that this is what happens in people with PTSD comes from astudy in which eight patients being treated for the problem were injected with CRF. Ordinarily, aninjection of CRF triggers a flood of ACTH, the hormone that streams through the body to triggercatecholamines. But in the PTSD patients, unlike a comparison group of people without PTSD, therewas no discernible change in levels of ACTH—a sign that their brains had cut back on CRF receptorsbecause they already were overloaded with the stress hormone. The research was described to me byCharles Nemeroff, a Duke University psychiatrist.
11. I interviewed Dr. Nemeroff in The New York Times (June 12, 1990).
12. Something similar seems to occur in PTSD: For instance, in one experiment Vietnam vets with aPTSD diagnosis were shown a specially edited 15-minute film of graphic combat scenes from themoviePlatoon. In one group, the vets were injected with naloxone, a substance that blocks endorphins;after watching the movie, these vets showed no change in their sensitivity to pain. But in the groupwithout the endorphin blocker, the men’s pain sensitivity decreased 30 percent, indicating an increasein endorphin secretion. The same scene had no such effect on veterans who did not have PTSD,suggesting that in the PTSD victims the nerve pathways that regulate endorphins were overly sensitiveor hyperactive——an effect that became apparent only when they were reexposed to somethingreminiscent of the original trauma. In this sequence the amygdala first evaluates the emotionalimportance of what we see. The study was done by Dr.Roger Pitman, a Harvard psychiatrist. As withother symptoms of PTSD, this brain change is not only learned under duress, but can be triggered onceagain if there is something reminiscent of the original terrible event. For example, Pitman found thatwhen laboratory rats were shocked in a cage, they developed the same endorphin-based analgesia foundin the Vietnam vets shownPlatoon. Weeks later,when the rats were put into the cages where they hadbeen shocked—but without any current being turned on—they once again became insensitive to pain,as they originally had been when shocked. See Roger Pitman, “Naloxone-Reversible AnalgesicResponse to Combat-Related Stimuli in Posttraumatic Stress Disorder,” Archives of General Medicine(June 1990). See also Hillel Glover, “Emotional Numbing: A Possible Endorphin- MediatedPhenomenon Associated with Post-Traumatic Stress Disorders and Other Allied PsychopathologicStates,” Journal of Traumatic Stress 5, 4 (1992).
13. The brain evidence reviewed in this section is based on Dennis Charney’s excellent article,“Psychobiologic Mechanisms.”
14. Charney, “Psychobiologic Mechanisms,” 300.
15. Role of prefrontal cortex in unlearning fear: In Richard Davidson’s study,volunteers had theirsweat response measured (a barometer of anxiety) while they heard a tone. followed by a loud,obnoxious noise. The loud noise triggered a rise in sweat. After a time, the tone alone was enough totrigger the same rise,showing that the volunteers had learned an aversion to the tone. As they continuedto hear the tone without the obnoxious noise, the learned aversion faded away—the tone soundedwithout any increase in sweat. The more active the volunteers’left prefrontal cortex, the more quicklythey lost the learned fear. In another experiment showing the prefrontal lobes’ role in getting over afear, lab rats—as is so often the case in these studies—learned to fear a tone paired with an electricshock. The rats then had what amounts to a lobotomy, a surgical lesion in their brain that cut off theprefrontal lobes from the amygdala. For the next several days the rats heard the tone without getting anelectric shock. Slowly, over a period ofdays, rats who have once learned to fear a tone will graduallylose their fear. Butfor the rats with the disconnected prefrontal lobes, it took nearly twice as longtounlearn the fear——suggesting a crucial role for the prefrontal lobes in managing fear and, moregenerally, in mastering emotional lessons. This experiment was done by Maria Morgan, a graduatestudent of Joseph LeDoux’s at the Center for Neural Science, New York University.
16. Recovery from PTSD: I was told about this study by Rachel Yehuda, a neurochemist and directorof the Traumatic Stress Studies Program at the Mt.Sinai School of Medicine in Manhattan. I reportedon the results in The New York Times (Oct. 6,1992).
17. Childhood trauma: Lenore Terr, Too Scared to Cry (New York:HarperCollins, 1990).
18. Pathway to recovery from trauma: Judith Lewis Herman, Trauma and Recovery (New York: BasicBooks, 1992).
19. “Dosing” of trauma: Mardi Horowitz, Stress Response Syndromes (Northvale, NJ: Jason Aronson,1986).
20. Another level at which relearning goes on, at least for adults, is philosophical. The eternal questionof the victim—”Why me?”—needs to be addressed. Being the victim of trauma shatters a person’s faiththat the world is a place that can be trusted, and that what happens to us in life is just—that is, that wecan have control over our destiny by living a righteous life. The answers to the victim’s conundrum, ofcourse, need not be philosophical or religious; the task is to rebuild a system of belief or faith thatallows living once again as though the world and the people in it can be trusted.
21. That the original fear persists, even if subdued, has been shown in studies where lab rats wereconditioned to fear a sound, such as a bell, when it was paired with an electric shock. Afterward, whenthey heard the bell they reacted with fear, even though no shock accompanied it. Gradually, over thecourse of a year(a very long time for a rat—about a third of its life), the rats lost their fearfulness of thebell. But the fear was restored in full force when the sound of the bell was once again paired with ashock. The fear came back in a single instant—but took months and months to subside. The parallel inhumans, of course, is when a traumatic fear from long ago, dormant for years, floods back in full forcewith some reminder of the original trauma.
22. Luborsky’s therapy research is detailed in Lester Luborsky and Paul Crits-Christoph,Understanding Transference: The CCRT Method (New York: BasicBooks, 1990).