Aronson T A, Whitaker-Azmitia P, Caraseti I
Department of Psychiatry and Behavioral Sciences, State University of New York, Stony Brook 1794-8101.
Biol Psychiatry. 1989 Feb 15;25(4):469-81. doi: 10.1016/0006-3223(89)90200-x.
Nine patients with panic disorder experienced a lactate-induced panic attack, whereas nine controls did not. Higher preinfusion anxiety levels and heart rates were associated with panic disorder, and high baseline anxiety ratings were associated with atypical, severe lactate-induced panic attacks. Nevertheless, it was difficult to reconcile patients' and controls' reactivity to lactate as entirely secondary to baseline differences. Subjects differed qualitatively in the types of specific symptoms experienced and quantitatively in their anxiety and heart rate responses. In most cases, panic began with various central perceptual changes; peripheral cardiovascular and autonomic symptoms followed later. No patient rated a lactate-induced panic attack as identical to a naturally occurring attack. Not only did specific symptoms differ in their severity and order of production, but lactate-induced panic lacked the typical fears of dying, going crazy, or losing control. The results suggest that though environmental effects, expectancy biases, and baseline psychological states play salient roles in modifying the experience of a lactate-induced panic attack, they do not fully account for lactate sensitivity. The relative role that biological, psychological, and conditioning factors play in lactate-induced panic is discussed.
9名惊恐障碍患者经历了乳酸诱发的惊恐发作,而9名对照组患者则未经历。输注前较高的焦虑水平和心率与惊恐障碍相关,而高基线焦虑评分与非典型、严重的乳酸诱发惊恐发作相关。然而,很难将患者和对照组对乳酸的反应性完全归因于基线差异。受试者在经历的特定症状类型上存在质的差异,在焦虑和心率反应上存在量的差异。在大多数情况下,惊恐发作始于各种中枢感知变化;随后出现外周心血管和自主神经症状。没有患者将乳酸诱发的惊恐发作评为与自然发生的发作相同。不仅特定症状在严重程度和产生顺序上不同,而且乳酸诱发的惊恐缺乏典型的对死亡、发疯或失去控制的恐惧。结果表明,尽管环境影响、预期偏差和基线心理状态在改变乳酸诱发惊恐发作的体验中起着重要作用,但它们并不能完全解释乳酸敏感性。本文讨论了生物学、心理学和条件因素在乳酸诱发惊恐中所起的相对作用。