创伤下的思考脑
《心理韧性》创伤下的思考脑,页面无弹窗的全文阅读!
受到创伤的人还会让情况变得更加复杂。这是因为在经历创伤之后，大脑负责认知、情绪和感觉运动水平的不同部分之间信息处理的整合过程常常会遭到损害。[44]而这放大了思考脑和生存脑之间的对立关系，同时为彻底恢复增加了额外的障碍。
人类从生存脑（杏仁核）到思考脑（前额叶皮层）的神经回路比反向回路更多，规模也更大。[45]这在进化上是说得通的，因为对威胁的快速评估和反应增加了我们的生存机会。此外，在慢性压力或创伤性压力之下，源自生存脑的神经回路会得到更多锻炼，而源自思考脑的神经回路则可能会受损或退化。总之，这两种不平衡有助于解释为什么当我们身处耐受窗之外时可能会发生生存脑劫持现象。
更重要的是，这两种不平衡也说明了为什么思考脑很难纠正生存脑受损的隐性记忆系统。这个被称为恐惧消退或创伤消退的过程，依赖于我们在慢性压力或创伤性压力中退化的思考脑回路。这种消退实际上是一种新记忆的生成，而非对我们现有记忆的消除。
在经历创伤事件之后，思考脑认为该事件已经过去，而我们生存了下来。由于思考脑知道事情已经过去，所以它通常会使用其思考、分析、计划、深思熟虑和决策的保护机制来保障我们未来的安全。它可能会对该事件进行分析，从中学习并为其赋予一定意义，它会谴责他人，进行自我批判，思考我们如何引发了该事件或制订计划来防止这样的事情再度发生。
换句话说，对思考脑而言，创伤已经过去，它的行动是利用其工具，继续前进。
思考脑的行动过程与生存脑的创伤后认知和保护计划完全相反。毕竟，生存脑认为创伤事件还在持续。因此，当生存脑感知到与未解记忆胶囊有关的征兆（包括通过点燃效应产生的应激唤醒的身体感觉）时，它会继续感知危险，调动应激机制。然而，矛盾的是，由于生存脑并不能支持思考脑认为创伤已经过去的“理性”认知，它们各自认知之间的不一致实际上可能会导致生存脑产生更加不安全的感觉。[46]
这就好像生存脑在说：“我发现身体里出现了种种应激唤醒现象。既然身体已被激活，那么一定有威胁，对吗？但我还没有看到威胁。因此，一定是有什么事蒙蔽了我，而危险可能比我想象的还要严重。”这种动因有助于解释为什么创伤幸存者常常觉得自己如履薄冰、提心吊胆。这正是他们的生存脑不自觉地想要将相对安全的外部环境和内心的危险感觉联系在一起的表现。
因此，这一过程通常会引发恶性循环也就不足为奇了，这会使受到创伤的生存脑将中性乃至积极的刺激视为威胁。实际上，受到创伤的幸存者可能会渐渐对体内各种形式的应激反应产生怀疑，哪怕是运动、跳舞或做爱时产生的愉悦的兴奋感。例如，在愉悦的事件中，思考脑可能会享受正在发生的事情，但同时受到创伤和过度警觉的生存脑则专注于寻找威胁来“解释”这种兴奋感。
遭遇创伤后，思考脑和生存脑对当前情况的理解存在巨大差异，生存脑会继续产生危险的感觉也就不难理解了。然而，由于思考脑认为创伤事件已经结束，所以它通常不理解身心系统为何会如此运作。
思考脑可能会尝试用对抗性的思考脑习惯去分析我们的行为和症状。例如，它可能会产生批判性的想法和比较性的想法，例如，“我现在应该结束这一切，我到底怎么了？其他人可能做得更糟糕。”思考脑也有可能会进行自我评判，产生内疚和羞愧的情绪。它可能会有焦虑的想法，担心这些症状永远不会消失或进一步恶化。所有这些对抗性的思考脑习惯只会加剧应激唤醒。
为了回应这些“分析”，思考脑可能会认为应激唤醒和失调症状是亟待解决的“问题”。这么做可能会导致思考脑控制，例如，对问题进行压制和隔离，咬咬牙，继续前进，奋勇向前。当我们生活在“自己的思想中”而脱离了情感、直觉和躯体时，思考脑控制的状况也会显现。
比如认知行为疗法、积极心理学、暴露疗法、其他谈话疗法、认知再评价或目标设定法等治疗手段可能也会在不经意间激励思考脑控制。思考脑主导的手段旨在通过强化自我，抑制应激唤醒，抑或让我们失去对未解记忆胶囊线索的敏感性来实现自上而下的自我调节，因为它认为应激唤醒才是需要解决的“问题”。
然而，如果这些手段没有与自下而上的处理过程相结合，那么在我们的耐受窗之内，生存脑便无法对受损的记忆系统进行更新。因此，仅仅使用这些技术可能会使受创伤者将他们的应激唤醒水平严格限制在他们狭窄的耐受窗中，从而避免触发他们未解决的记忆胶囊。[47]然而，与此同时，他们还是处在隔离状态，与他们自身相信创伤还在继续的那一部分相互分离。反过来，生存脑和身体继续用未解的记忆胶囊覆盖当前状态，它们无意识地依赖默认创伤防御程序，并通过点燃效应制造越来越严重的失调症状。
因此，正如创伤治疗医师帕特·奥格登和她的同事解释的那样，尽管思考脑主导的手段“为过度兴奋提供了有效管理，显著缓解了症状，但它们可能无法彻底解决这一问题”。[48]
可以肯定的是，在特定情况下，思考脑可以在短时间内非常熟练地发挥控制作用。尽管如此，这些手段本身并不能促进拓宽耐受窗所需的彻底恢复。实际上，采用这些手段时，思考脑可能会感到更有控制力，而生存脑对无助和缺乏控制力的感觉可能还将持续。因此，长期依赖这些方法可能会使未解的记忆胶囊永续下去，同时增加非稳态负荷。
最终，思考脑的控制可能也会积极抑制生存脑对恢复的尝试。我们大多数人从未被教导过如何在身心系统中释放应激唤醒。（你将在第三部分了解到这方面的内容。）因此，当这些感觉和习惯自发产生时，我们可能会推翻和抑制它们，特别是当它们落入思考脑的叙事和文化范式时，比如“男孩不哭”。
思考脑的控制作用越发极端，生存脑的应激唤醒水平就越高，它可能会向思考脑传递这样的信息：“我现在不安全！”为了让它的信息能够传递过去，它采取了生存脑劫持手段（比如闪回、噩梦以及呕吐在键盘上），这也是失调的一种表现。作为回应，思考脑会加倍抑制、隔离，让人咬紧牙关，继续前进，无视生存脑发出的信号。实际上，它会产生这样的想法：“我到底怎么了？这些都是过去的事了。我现在应该已经跨过这个坎了。”
每当思考脑阻碍了生存脑试图恢复的努力，它就会加剧我们的失调症状。更重要的是，它还会进一步肯定和重建应激唤醒与生存脑无助感之间的联系，这种神经生物学上的重要耦合正是创伤性压力的特点。实际上，生存脑会将“我无法成功保护自己”的创伤思维泛化为“我无法成功恢复”的想法。这种对彻底康复的无助感进一步锁定了创伤模式，造成恶性循环。
对经历过创伤的人来说，这是一个难解的死结：体内的应激反应、未解的记忆胶囊、在创伤事件中采用的不完善或不成功的默认防御手段和关系策略以及当前无法彻底恢复的习得性无助。在解开这个死结之前，生存脑和身体会继续认为创伤事件仍在进行之中，因此它们会依赖创伤中的默认程序。
然而，由于思考脑和生存脑对之前的创伤有着相当不同的理解，所以思考脑常常会在不知不觉中成为从未实现过的全面恢复的主要障碍。相反，为了应对日益严重的失调症状，大多数受过创伤的人都会采用一系列被社会接受的行为来应对——然而可悲的是，这么做只会进一步缩小耐受窗。
在开始下一章之前，我想鼓励你带着不加评判的好奇心，回忆你经历过的思考脑控制，比如隔离或生存脑劫持，如闪回或点燃效应。在你的笔记中，你可以问问自己，这些心理习惯是否是由特定的情况、人际关系或记忆所触发的。当这些习惯被触发时，你通常又是如何应对它们的？
治愈思考脑和生存脑之间的对立关系的第一步是意识到它的存在。在理解了它的神经生物学动因之后，随着时间的推移，我们便可以促进生存脑实现彻底的恢复，同时消除它与思考脑之间的对立关系。
[1]有关系统1思维的特征，可参考： Daniel Kahneman, Thinking, Fast and Slow (New York: Macmillan, 2011), 105。
[2]Pat Ogden, Kekuni Minton, and Clare Pain, Trauma and the Body: A Sensorimotor Approach to Psychotherapy (New York: Norton, 2006), chap. 1;Robert C. Scaer, The Trauma Spectrum: Hidden Wounds and Human Resiliency(New York: Norton, 2005), chap. 2; Stephen W. Porges, The Polyvagal Theory:Neurophysiological Foundations of Emotions, Attachment, Communication,and Self-Regulation (New York: Norton, 2011), chaps. 1, 3.
[3]Scaer, The Trauma Spectrum, 40-42.
[4]Scaer, The Trauma Spectrum, 40-42; Robert M. Sapolsky, Why Zebras Don't Get Ulcers, 3rd ed. (New York: Holt, 2004), chap. 15; J. Douglas Bremner,Does Stress Damage the Brain?: Understanding Trauma-Related Disorders from a Mind-Body Perspective (New York: Norton, 2005), chap. 4; Bruce S. McEwen and Elizabeth Norton Lasley, The End of Stress as We Know It(Washington, D.C.: Joseph Henry, 2002), 108-110.
[5]Sapolsky, Why Zebras Don't Get Ulcers, 320-322; Scaer, The Trauma Spectrum, 40-42; J. LeDoux, “The Emotional Brain, Fear, and the Amygdala,”Cellular and Molecular Neurobiology 23, no. 4-5 (2003): 727-738; McEwen and Lasley, The End of Stress as We Know It, chap. 7; Bremner, Does Stress Damage the Brain?, chap. 4.
[6]Paul D. MacLean, The Triune Brain in Evolution: Role in Paleocerebral Functions (New York: Plenum, 1990); Ogden et al., Trauma and the Body,chap. 1.
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[9]Hofmann et al. “Executive Functions and Self-Regulation.”有关睡眠不足对执行功能的影响可参考：L. K. Barger et al., “Neurobehavioral, Health,and Safety Consequences Associated with Shift Work in Safety-Sensitive Professions,” Curren Neurology and Neuroscience Reports 9, no. 2 (2009):155-164。
[10]Heatherton and Wagner, “Cognitive Neuroscience of Self-Regulation Failure”;Hofmann et al., “Executive Functions and Self-Regulation.”
[11]Scaer, The Trauma Spectrum, 38-39; Bremner, Does Stress Damage the Brain?, 45-47.
[12]Scaer, The Trauma Spectrum, 38; Pe et al., “The Cognitive Building Blocks of Emotion Regulation”, Hofmann et al., “Working Memory Capacity and SelfRegulatory Behavior”.
[13]Sapolsky, Why Zebras Don't Get Ulcers, chap. 10.
[14]McEwen and Lasley, The End of Stress as We Know It, 130; E. R. De Kloet et al., “Brain Corticosteroid Receptor Balance in Health and Disease,” Endocrine Review 19, no. 3 (1998): 269-301.
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[16]有关这一动因的精彩评述，可参考：McEwen and Lasley, The End of Stress as We Know It, chap. 7; Bremner, Does Stress Damage the Brain?,chap. 4; Sapolsky, Why Zebras Don't Get Ulcers, chap. 10。
[17]J. J. Vasterling et al., “Neuropsychological Outcomes of Army Personnel Following Deployment to the Iraq War,” Journal of the American Medical Association 296, no. 5 (2006): 519-529.
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[19]Scaer, The Trauma Spectrum, 62-64; Sapolskv, Why Zebras Don't Get Ulcers,chap. 1; Kavanagh, Stress and Performance, 31.
[20]S. J. Lupien et al., “Cortisol Levels during Human Aging Predict Hippocampal Atrophy and Memory Deficits,” Nature Neuroscience 1 (1998): 69-73;Sapolsky, Why Zebras Don't Get Ulcers, chap. 10. 幸运的是，其他有关动物和人类的研究表明，皮质醇升高的影响不会造成永久性伤害。当皮质醇水平回到正常状态时，海马体也会开始恢复正常大小，参见：McEwen and Lasley, The End of Stress as We Know It, chap. 7. 升高的皮质醇水平与创伤后应激障碍之间的关系并没有那么明确，很多患有创伤后应激障碍的人的皮质醇水平有时候较低，但他们的HPA轴对应激反应依然高度敏感，因此研究人员通常认为创伤后应激障碍导致的海马体体积损失是不可逆的。然而一些研究表明，创伤后应激障碍导致的海马体体积损失是可以得到还原的，参见：E. Vermetten et al., “LongTerm Treatment with Paroxetine Increases Verbal Declarative Memory and Hippocampal volume in Posttraumatic Stress Disorder,” Biological Psychiatry 54 (2003): 693-702; Bremner, Does Stress Damage the Brain?, 60-62, 115119. 其他研究则指出了相反的因果关系：在经历压力性事件之前，海马体和记忆方面出现的小问题会增加遭遇创伤后出现应激障碍的风险，例如，在经历童年期不良经历之后，参见：Marx et al., “The Infuence of Pre-Deployment Neurocognitive Functioning”; R. A. Parslow and A. F. Jorm “Pretrauma and Posttrauma Neurocognitive Functioning and PTSD Symptoms in a Community Sample of Young Adults,” American Journal of Psychiatry 164, no. 3 (2007): 509-515; Sapolsky, Why Zebras Don't Get Ulcers, chap. 10, esp. 222。
[21]K. Cho, “Chronic ‘Jet Lag’ Produces Temporal Lobe Atrophy and Spatial Cognitive Deficits,” Nature Neuroscience 4 (2001): 567-568.
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[23]Sapolsky, Why Zebras Don't Get Ulcers, 221.
[24]Bremner, Does Stress Damage the Brain? 60-62, 115-119.
[25]Bremner, Does Stress Damage the Bnain?, chap. 4; Kavanagh, Stress and Performama, 16-19; McEwen and Lasley, The End of Sress as We Know It,chap. 7.
[26]Daniel J. Siegel, The Developing Mind: How Relationships and the Brain Interact to Shape Who We Are (New York: Guilford, 1999), 253; Ogden et al.,Trauma and the Body, chap. 2.
[27]Porges, The Polyvagal Theory, chap. 1; Ogden et al., Trauma and the Body,chap. 2; Bremner, Does Sress Damage the Brain?, chap. 4; McEwen and Lasley, The End of Stress as We Know lt, chap. 7; Sapolsky, Why Zebras Don't Get Ulcers, chaps. 10, 15.
[28]Kavanagh, Stress and Performance,16-17.
[29]Porges, The Polyvagal Theory, chap. 1; E. A. Scanley, “War Duration and the Micro-Dynamics of Decision-Making under Stress,” Polity 50, no.2 (2018):178-200; J. Renshon, J. J. Lee, and D. Tingley, “Emotions and the MicroFoundations of Commitment Problems,” International Organization 71, no.S1 (2017): S189-S218.
[30]Kavanagh, Stress and Performance, 17-18; Karl E. Weick, Sensemaking in Organizations (New York: Sage, 1995), 129.
[31]Kahneman, Thinking, Fast and Slow; Elizabeth A. Stanley, Paths to Peace: Domestic Coalition Shifts, War Termination and the Korean War (Stanford,CA: Stanford University Press, 2009), chap. 2; Kavanagh, Stress and Perfornamce, 17-19; Scott Sigmund Gartner, Strategic Assessment in War(New Haven, CT: Yale University Press, 1999).
[32]R. F. Baumeister et al., “Bad Is Stronger Than Good,” Review of General Psychology 5, no. 4 (2001): 323-370; P. Rozin and E. B. Royzman,“Negativity Bias, Negativity Dominance, and Contagion,” Personality and Social Psychology Review 5, no. 4 (2001): 296-320.
[33]Stanley, “War Duration”; Kavanagh, Stress and Performance, 17-20;Kahneman, Thinking, Fast and Slow.
[34]Scaer, The Trauma Spectrum, 58-59, 132-133.
[35]Scaer, The Trauma Spectrum, chap. 3; Ogdenet al., Trauma and the Body, 2022, 86-87.
[36]Scaer, The Trauma Spectrum, 42, 95, chap. 3; Ogden et al., Trauma and the Body, 34-36, 86-87.
[37]Scaer, The Trauma Spectrum, chap. 3, 42; Ogden et al., Trauma and the Body, 18-23, 86-87, 104-105; B. A. van der Kolk, “Clinical Implications of Neuroscience Research in PTSD,” Annals of the New York Academy of Sciences 1071, no. 1 (2006): 277-293.
[38]Scaer, The Trauma Spectrum, 59-64; Robert C. Scaer, The Body Bears the Burden: Trauma, Dissociation, and Disease, 3rd ed. (New York: Routledge,2014), 91-95.
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