The Human Amygdala and the Induction and Experience of Fear
Abstract
Although clinical observations suggest that humans with amygdala damage have abnormal fear reactions and a reduced experience of fear [1-3], these impressions have not been systematically investigated. To address this gap, we conducted a new study in a rare human patient, SM, who has focal bilateral amygdala lesions [4]. To provoke fear in SM, we exposed her to live snakes and spiders, took her on a tour of a haunted house, and showed her emotionally evocative films. On no occasion did SM exhibit fear, and she never endorsed feeling more than minimal levels of fear. Likewise, across a large battery of self-report questionnaires, 3 months of real-life experience sampling, and a life history replete with traumatic events, SM repeatedly demonstrated an absence of overt fear manifestations and an overall impoverished experience of fear. Despite her lack of fear, SM is able to exhibit other basic emotions and experience the respective feelings. The findings support the conclusion that the human amygdala plays a pivotal role in triggering a state of fear and that the absence of such a state precludes the experience of fear itself.
Additional Information
© 2011 Elsevier Ltd. Received 4 October 2010; revised 16 November 2010; accepted 16 November 2010. Published online: December 16, 2010. We are greatly indebted to SM for her continued commitment to brain research. We would also like to thank Christopher Kovach for his invaluable help during some of the testing and Joel Bruss for his assistance with SM's brain scans. This research was supported by grants from the National Institutes of Health (National Institute of Neurological Disorders and Stroke P50 NS19632, National Institute on Drug Abuse R01 DA022549, and National Institute for Mental Health R01 MH080721) and a National Science Foundation Graduate Research Fellowship.Attached Files
Accepted Version - nihms254004.pdf
Supplemental Material - mmc1.pdf
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Additional details
- PMCID
- PMC3030206
- Eprint ID
- 22602
- DOI
- 10.1016/j.cub.2010.11.042
- Resolver ID
- CaltechAUTHORS:20110302-102609291
- NIH
- P50 NS19632
- NIH
- R01 DA022549
- NIH
- R01 MH080721
- NSF Graduate Research Fellowship
- Created
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2011-03-03Created from EPrint's datestamp field
- Updated
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2021-11-09Created from EPrint's last_modified field