Altered experience of emotion following bilateral amygdala damage - PubMed (original) (raw)

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Altered experience of emotion following bilateral amygdala damage

Daniel Tranel et al. Cogn Neuropsychiatry. 2006 May.

Abstract

It has been well established that the amygdala is critical for processing various aspects of emotion, and in particular, for the perception of negative emotions such as fear. Perhaps the strongest evidence for this conclusion in humans comes from an extensive series of investigations in patient SM, an extremely rare neurological patient who has complete, focal bilateral amygdala damage. One question that has remained unanswered, however, is whether SM has a normal phenomenological experience of emotion, especially negative emotion. To explore this issue, we designed a study in which two experienced clinical psychologists conducted "blind" interviews of SM (the psychologists were not provided any background information regarding SM), with a special emphasis regarding the nature of her emotional experience. Both of them reached the conclusion that SM expressed a normal range of affect and emotion, and neither felt that SM warranted a DSM-IV diagnosis. However, they both noted that SM was remarkably dispassionate when relating highly emotional and traumatic life experiences, and they noted that she did not seem to have a normal sense of distrust and "danger". To the psychologists, SM came across as a "survivor", as being "resilient" and even "heroic" in the way that she had dealt with adversity in her life. In the full light of SM's neurological and neuropsychological profile, however, these observations reflect the fact that SM is missing from the experiences in her life some of the deepest negative emotions, in a manner that parallels her defect in perceiving such emotions in external stimuli. These findings have interesting parallels with recent animal work (cf. Bauman, Lavenex, Mason, Capitanio, & Amaral, 2004a), and they provide valuable insights into the emotional life of an individual with complete bilateral amygdala damage.

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