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Published May 11, 2004 | Published
Journal Article Open

Impaired spontaneous anthropomorphizing despite intact perception and social knowledge


Humans spontaneously imbue the world with social meaning: we see not only emotions and intentional behaviors in humans and other animals, but also anger in the movements of thunderstorms and willful sabotage in crashing computers. Converging evidence supports a role for the amygdala, a collection of nuclei in the temporal lobe, in processing emotionally and socially relevant information. Here, we report that a patient with bilateral amygdala damage described a film of animated shapes (normally seen as full of social content) in entirely asocial, geometric terms, despite otherwise normal visual perception. Control tasks showed that the impairment did not result from a global inability to describe social stimuli or a bias in language use, nor was a similar impairment observed in eight comparison subjects with damage to orbitofrontal cortex. This finding extends the role of the amygdala to the social attributions we make even to stimuli that are not explicitly social and, in so doing, suggests that the human capacity for anthropomorphizing draws on some of the same neural systems as do basic emotional responses.

Additional Information

© 2004 the National Academy of Sciences. Edited by James L. McGaugh, University of California, Irvine, CA, and approved March 30, 2004 (received for review December 10, 2003). We are grateful to David Kemmerer for the video and for discussions regarding its use, to Daniel Tranel, Josh Greene, Martha Farah, Lesley Fellows, Luiz Pessoa, Susan Carey, and two anonymous reviewers for comments on earlier versions of this manuscript, to Tony Buchanan and Benjamin Lewis for help in collecting data on the picture book task, to Jamie Pennebaker for help with the LIWC analyses, and to Kodi Scheer, Matt Karafin, Jocelyn Spoon, and Jennifer Shultz for coding of specific questionnaire items. This work was supported by National Institute of Neurological Disorders and Stroke Program Project Grant NS19632. A.S.H. was supported by National Institutes of Health Grant T32-NS07413 at the Children's Hospital of Philadelphia during preparation of the final manuscript. This paper was submitted directly (Track II) to the PNAS office.

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