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In psychoanalytic theory, signal anxiety heralds the imminent emergence into consciousness of an unacceptable thought. In terms of therapeutic technique, psychoanalysis has long distinguished itself from cognitive behavioral therapy in emphasizing the importance of uncovering these thoughts, working with them, and rendering them tolerable, rather than on enhancing the patient's suppressive capacity. In this sense, the anxiety is taken as a useful, but in itself unproblematic, marker of fearful thoughts that must be processed.
The possibility that patients differ genetically in their tendency to label internal stimuli as anxiety provoking throws some doubt on this formulation. In short, what if the problem with signal anxiety is not the underlying thought, or the signal itself, but, rather, the association between the two? This would carve out a middle ground between pharmacological strategies that simply seek to dampen anxiety symptoms and analytic ones that seek to explore anxious ideation. The neu-roanatomical analog of this hypothesis is the following: In analytic theory, amygdala activation signals the association of a stimulus with danger (which precedes, but is distinct from, the mobilization of autonomic arousal or instrumental responses). The amygdala activation per se is not considered problematic; what is problematic is the association of the stimulus with danger, occurring in memory-association regions such as the hippocampus.
In analytic theory, exploring this association may allow decoupling of the stimulus from the danger association through improved information processing in memory formation and retrieval regions. For example, a stimulus that only deserves moderate concern may be falsely tagged with high-danger status; the association mechanism may need to be fine-tuned to allow association with only moderate danger. In a wonderful recent study, Tsetsenis and colleagues exploited the known role of serotonergic (5HT) function in anxiety-dampening. They b