ERIC Number: EJ730488
Record Type: Journal
Publication Date: 2004-Jun
Pages: 11
Abstractor: Author
Reference Count: 0
ISBN: N/A
ISSN: ISSN-0278-2626
The Roles of Orbital Frontal Cortex in the Modulation of Antisocial Behavior
Blair, R. J. R.
Brain and Cognition, v55 n1 p198-208 Jun 2004
This article considers potential roles of orbital frontal cortex in the modulation of antisocial behavior. Two forms of aggression are distinguished: reactive aggression elicited in response to frustration/threat and goal directed, instrumental aggression. It is suggested that orbital frontal cortex is directly involved in the modulation of reactive aggression. It is argued that orbital frontal cortex does not "inhibit'' reactive aggression but rather may both increase or decrease its probability as a function of social cues present in the environment. Early dysfunction in this function of orbital frontal cortex may be linked to the development of Borderline Personality Disorder. Instrumental aggression is linked to a fundamental failure in moral socialization. However, the available data suggest that the amygdala, but not orbital frontal cortex, is required for functions such as aversive conditioning and passive avoidance learning that are necessary for moral socialization. Psychopathic individuals who present with significant instrumental aggression, are impaired in aversive conditioning and passive avoidance learning and show evidence of amygdala dysfunction. Orbital frontal cortex and the amygdala are involved in response reversal where instrumental responses must be reversed following contingency change. Impairments in response reversal are also seen in psychopathic individuals. However, it remains unclear whether impairment in response reversal per se is associated with antisocial behavior.
Descriptors: Antisocial Behavior, Aggression, Brain, Responses, Behavior Disorders, Neurological Impairments
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Publication Type: Journal Articles; Reports - Research
Education Level: N/A
Audience: N/A
Language: English
Sponsor: N/A
Authoring Institution: N/A
Identifiers: N/A

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