Literature DB >> 22563006

Early sensory-perceptual processing deficits for affectively valenced inputs are more pronounced in schizophrenia patients with a history of violence than in their non-violent peers.

Pierfilippo De Sanctis1, John J Foxe, Pal Czobor, Glenn R Wylie, Stephanie M Kamiel, Jessica Huening, Mike Nair-Collins, Menahem I Krakowski.   

Abstract

Individuals with schizophrenia are more prone to violent behaviors than the general population. It is increasingly recognized that processing of emotionally valenced stimuli is impaired in schizophrenia, a deficit that may play a role in aggressive behavior. Our goal was to establish whether patients with a history of violence would show more severe deficits in processing emotionally valenced inputs than non-violent patients. Using event-related potentials, we measured how early during processing of emotional valence, evidence of aberrant function was observed. A total of 42 schizophrenia patients (21 with history of violence; 21 without) and 28 healthy controls were tested. Participants performed an inhibitory control task, making speeded responses to pictorial stimuli. Pictures occasionally repeated twice and participants withheld responses to these repeats. Valenced pictures from the International Affective Picture System were presented. Results in controls showed modulations during the earliest phases of sensory processing (<100 ms) for negatively valenced pictures. A cascade of modulations ensued, involving sensory and perceptual processing stages. In contrast, neither schizophrenia group showed early differentiation. Non-violent patients showed earliest modulations beginning ∼150 ms. For violent patients, however, earliest modulations were further delayed and highly attenuated. The current study reveals sensory-perceptual processing dysfunction for negatively valenced inputs, which is particularly pronounced in aggressive patients.

Entities:  

Keywords:  Schizophrenia; amygdala; emotion; event-related potential; violence

Mesh:

Year:  2012        PMID: 22563006      PMCID: PMC3739916          DOI: 10.1093/scan/nss052

Source DB:  PubMed          Journal:  Soc Cogn Affect Neurosci        ISSN: 1749-5016            Impact factor:   3.436


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