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Instrumental learning and relearning in individuals with psychopathy and in patients with lesions involving the amygdala or orbitofrontal cortex

dc.contributor.authorMitchell, Derek
dc.contributor.authorFine, Cordelia
dc.contributor.authorRichell, RA
dc.contributor.authorNewman, Chris
dc.contributor.authorLumsden, John
dc.contributor.authorBlair, Kerena
dc.contributor.authorBlair, James
dc.date.accessioned2015-12-07T22:17:03Z
dc.date.issued2006
dc.date.updated2015-12-07T08:01:45Z
dc.description.abstractPrevious work has shown that individuals with psychopathy are impaired on some forms of associative learning, particularly stimulus-reinforcement learning (Blair et al., 2004; Newman & Kosson, 1986). Animal work suggests that the acquisition of stimulus-reinforcement associations requires the amygdala (Baxter & Murray, 2002). Individuals with psychopathy also show impoverished reversal learning (Mitchell, Colledge, Leonard, & Blair, 2002). Reversal learning is supported by the ventrolateral and orbitofrontal cortex (Rolls, 2004). In this paper we present experiments investigating stimulus-reinforcement learning and relearning in patients with lesions of the orbitofrontal cortex or amygdala, and individuals with developmental psychopathy without known trauma. The results are interpreted with reference to current neurocognitive models of stimulus-reinforcement learning, relearning, and developmental psychopathy.
dc.identifier.issn0894-4105
dc.identifier.urihttp://hdl.handle.net/1885/18360
dc.publisherAmerican Psychological Association
dc.sourceNeuropsychology
dc.subjectKeywords: adult; amygdaloid nucleus; article; brain damage; brain depth stimulation; case report; cognition; developmental disorder; human; learning; male; medical instrumentation; orbital cortex; priority journal; psychopathy; reinforcement; traumatic brain injury Acquired sociopathy; Amygdala lesion; Instrumental learning; Orbitofrontal cortex lesion; Psychopathy
dc.titleInstrumental learning and relearning in individuals with psychopathy and in patients with lesions involving the amygdala or orbitofrontal cortex
dc.typeJournal article
local.bibliographicCitation.issue3
local.bibliographicCitation.lastpage289
local.bibliographicCitation.startpage280
local.contributor.affiliationMitchell, Derek, National Institutes of Health
local.contributor.affiliationFine, Cordelia, College of Arts and Social Sciences, ANU
local.contributor.affiliationRichell, RA, Imperial College (London)
local.contributor.affiliationNewman, Chris, University of London
local.contributor.affiliationLumsden, John, Broadmoor Hospital
local.contributor.affiliationBlair, Kerena, National Institutes of Health
local.contributor.affiliationBlair, James, National Institutes of Health
local.contributor.authoruidFine, Cordelia, u4264863
local.description.embargo2037-12-31
local.description.notesImported from ARIES
local.identifier.absfor179999 - Psychology and Cognitive Sciences not elsewhere classified
local.identifier.absfor110999 - Neurosciences not elsewhere classified
local.identifier.absseo970106 - Expanding Knowledge in the Biological Sciences
local.identifier.absseo970117 - Expanding Knowledge in Psychology and Cognitive Sciences
local.identifier.ariespublicationu4264863xPUB4
local.identifier.citationvolume20
local.identifier.doi10.1037/0894-4105.20.3.280
local.identifier.scopusID2-s2.0-33745109862
local.type.statusPublished Version

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