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Journal Article

Citation

Dellacherie D, Hasboun D, Baulac M, Belin P, Samson S. Neuropsychologia 2011; 49(4): 618-629.

Affiliation

Laboratoire de Neurosciences Fonctionnelles et Pathologies CNRS UMR 8160, University of Lille - Nord de France, France; Epilepsy Unit, La Salpêtrière Hospital, Paris, France.

Copyright

(Copyright © 2011, Elsevier Publishing)

DOI

10.1016/j.neuropsychologia.2010.11.008

PMID

21108955

Abstract

It has been reported that bilateral amygdala damage in humans compromises the recognition of fear and anger in nonverbal vocalizations (Scott et al., 1997). We addressed the possibility that unilateral temporal lobe damage might be sufficient to impair fear recognition (but not other emotions) in voices. For this purpose, we tested patients after left (n=10) or right (n=8) medial temporal lobe resection for the relief of intractable epilepsy using a set of nonverbal vocalizations (Belin, Fillion-Bilodeau, & Gosselin, 2008). To focus more narrowly on the role of amygdala subparts, we differentiated patients with complete amygdala damage vs. damage limited to the basolateral complex of the amygdala. The results confirmed for the first time that unilateral amygdala lesion including the basolateral complex can selectively impair recognition of fear and surprise expressed by voices, supporting the notion that the amygdala is a multimodal structure. Interestingly, this impairment was observed in patients with incomplete resection of the amygdala that spared the central nucleus and the corticomedial complex, suggesting that a resection of the basolateral complex is sufficient to affect fear recognition. Given that fear has often been considered as a precursor of anxiety, we also investigated the effect of such lesions on self-reported anxiety. The same patients appeared to be less anxious than control participants in their mood questionnaires. The association of impaired fear perception and decreased anxiety level is considered in the light of recent human and animal data, providing support for a neurobiological basis of mood changes in patients with unilateral temporal lobe damage.


Language: en

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