A model of differential amygdala activation in psychopathy

Caroline Moul*, Simon Killcross, Mark R. Dadds

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

122 Citations (Scopus)


This article introduces a novel hypothesis regarding amygdala function in psychopathy. The first part of this article introduces the concept of psychopathy and describes the main cognitive and affective impairments demonstrated by this population; that is, a deficit in fear-recognition, lower conditioned fear responses and poor performance in passive avoidance, and response-reversal learning tasks. Evidence for amygdala dysfunction in psychopathy is considered with regard to these deficits; however, the idea of unified amygdala function is untenable. A model of differential amygdala activation in which the basolateral amygdala (BLA) is underactive while the activity of the central amygdala (CeA) is of average to above average levels is proposed to provide a more accurate and up-to-date account for the specific cognitive and emotional deficits found in psychopathy. In addition, the model provides a mechanism by which attentional-based models and emotion-based models of psychopathy can coexist. Data to support the differential amygdala activation model are provided from studies from both human and animal research. Supporting evidence concerning some of the neurochemicals implicated in psychopathy is then reviewed. Implications of the model and areas of future research are discussed.

Original languageEnglish
Pages (from-to)789-806
Number of pages18
JournalPsychological Review
Issue number4 A
Publication statusPublished - 2012
Externally publishedYes


  • Basolateral amygdala
  • Central amygdala
  • Model
  • Psychopathy


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