A differential neural response to threatening and non-threatening negative facial expressions in paranoid and non-paranoid schizophrenics

Phillips, Mary L.; Williams, Lea M.; Senior, Carl; Bullmore, Edward T.; Brammer, Michael; Andrew, Christopher; Williams, Steven; David, Anthony S.

doi:10.1016/s0925-4927(99)00031-1

Cited by 273 publications

(198 citation statements)

References 55 publications

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“…The SCZ high-risk RISK + group, however, failed to demonstrate this normal taskrelated deactivation. In SCZ, abnormally reduced responses of the amygdala to emotional vs neutral stimuli have previously been reported (Schneider et al, 1998;Phillips et al, 1999;Gur et al, 2002;Williams et al, 2004;Romaniuk et al, 2010), proposed to derive from an increased response to neutral stimuli (Schwartz et al, 2003;Holt et al, 2006;Surguladze et al, 2006;Hall et al, 2008;Romaniuk et al, 2010). Together with behavioral studies showing deficits in emotion recognition, it is suggested there is an overactivation and misinterpretation of ambiguous stimuli as being emotionally salient.…”

Section: Discussionmentioning

confidence: 87%

Impact of a microRNA MIR137 Susceptibility Variant on Brain Function in People at High Genetic Risk of Schizophrenia or Bipolar Disorder

Whalley

Papmeyer

Romaniuk

et al. 2012

Neuropsychopharmacol

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A recent 'mega-analysis' combining genome-wide association study data from over 40 000 individuals identified novel genetic loci associated with schizophrenia (SCZ) at genome-wide significance level. The strongest finding was a locus within an intron of a putative primary transcript for microRNA MIR137. In the current study, we examine the impact of variation at this locus (rs1625579, G/T; where T is the common and presumed risk allele) on brain activation during a sentence completion task that differentiates individuals with SCZ, bipolar disorder (BD), and their relatives from controls. We examined three groups of individuals performing a sentence completion paradigm: (i) individuals at high genetic risk of SCZ (n ¼ 44), (ii) individuals at high genetic risk of BD (n ¼ 90), and (iii) healthy controls (n ¼ 81) in order to test the hypothesis that genotype at rs1625579 would influence brain activation. Genotype groups were assigned as 'RISKÀ' for GT and GG individuals, and 'RISK + ' for TT homozygotes. The main effect of genotype was significantly greater activation in the RISKÀ individuals in the posterior right medial frontal gyrus, BA 6. There was also a significant genotype*group interaction in the left amygdala and left pre/postcentral gyrus. This was due to differences between the controls (where individuals with the RISKÀ genotype showed greater activation than RISK + subjects) and the SCZ high-risk group, where the opposite genotype effect was seen. These results suggest that the newly identified SCZ locus may influence brain activation in a manner that is partly dependent on the presence of existing genetic susceptibility for SCZ.

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Section: Discussionmentioning

confidence: 87%

Impact of a microRNA MIR137 Susceptibility Variant on Brain Function in People at High Genetic Risk of Schizophrenia or Bipolar Disorder

Whalley

Papmeyer

Romaniuk

et al. 2012

Neuropsychopharmacol

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“…Further, only minimal differences in social cognition have been observed between individuals with autism and those with schizophrenia when the latter group was higher in paranoid symptoms (Craig et al, 2004;Pilowsky et al, 2000). Thus, based on this evidence and in conjunction with work suggesting greater amygdala activation in NP-SCZ relative to P-SCZ (Phillips et al, 1999;Williams et al, 2004), we tentatively hypothesized that the ASD and P-SCZ groups would show less amygdala activation than the NP-SCZ group.…”

Section: Introductionmentioning

confidence: 78%

“…complex social judgments; Craig et al, 2004;Pilowsky et al, 2000); however, our understanding of these deficits, and the potential similarities between disorders, remains incomplete. Specifically, behavioral findings are complicated by heterogeneity within disorders, particularly in schizophrenia, as individuals with persecutory delusions perform differently both at behavioral and neural levels on social cognitive tasks relative to individuals without persecutory delusions (Bentall et al, 2001;Davis and Gibson, 2000;Phillips et al, 1999;Ueno et al, 2004;Williams et al, 2004). Additionally, despite evidence of abnormal activation in the neural systems of social cognition in schizophrenia and autism (Pinkham et al, 2003;Pelphrey et al, 2004), no studies have used fMRI to directly compare the neural substrates underlying social cognitive performance in both disorders.…”

Section: Introductionmentioning

confidence: 99%

“…trustworthiness) of faces in four groups: highfunctioning individuals with autism spectrum disorders (ASD), paranoid individuals with schizophrenia (P-SCZ), non-paranoid individuals with schizophrenia (NP-SCZ), and nonclinical healthy controls. As previous research has demonstrated significantly greater amygdala activation in non-paranoid, relative to paranoid individuals with schizophrenia (Phillips et al, 1999;Williams et al, 2004), two separate groups of patients with schizophrenia were recruited in order to provide the most comprehensive comparison with ASD and to account for known differences between schizophrenia subgroups. Further, decisions of trustworthiness were employed due to previous work demonstrating that these judgments fully engage the neural regions implicated in social cognition in healthy individuals (Winston et al, 2002) and to the likelihood that these judgments would be particularly salient in assessing differences between paranoid and non-paranoid individuals.…”

Section: Introductionmentioning

confidence: 99%

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Neural bases for impaired social cognition in schizophrenia and autism spectrum disorders

Pinkham

Hopfinger

Pelphrey

et al. 2008

Schizophrenia Research

342

279

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Schizophrenia and autism both feature significant impairments in social cognition and social functioning, but the specificity and mechanisms of these deficits remain unknown. Recent research suggests that social cognitive deficits in both disorders may arise from dysfunctions in the neural systems that underlie social cognition. We explored the neural activation of discrete brain regions implicated in social cognitive and face processing in schizophrenia subgroups and autism spectrum disorders during complex social judgments of faces. Twelve individuals with autism spectrum disorders (ASD), 12 paranoid individuals with schizophrenia (P-SCZ), 12 non-paranoid individuals with schizophrenia (NP-SCZ), and 12 non-clinical healthy controls participated in this cross sectional study. Neural activation, as indexed by blood oxygenation level dependent (BOLD) contrast, was measured in a priori regions of interest while individuals rated faces for trustworthiness. All groups showed significant activation of a social cognitive network including the amygdala, fusiform face area (FFA), superior temporal sulcus (STS), and ventrolateral prefrontal cortex (VLPFC) while completing a task of complex social cognition (i.e. trustworthiness judgments). ASD and P-SCZ individuals showed significantly reduced neural activation in the right amygdala, FFA, and left VLPFC as compared to controls and in the left VLPFC as compared to NP-SCZ individuals during this task. These findings lend support to models hypothesizing well-defined neural substrates of social cognition and suggest a specific neural mechanism that may underlie social cognitive impairments in both autism and paranoid schizophrenia.

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“…Cognitive or evaluative processing of facial expressions seem to attenuate this amygdala response (Phillips et al, 1998;Hariri et al, 2000) and possibly shift the activation leftward (Phelps et al, 2001). Schizophrenia patients tend to show less activation overall when making an emotional discrimination and fail to recruit limbic regions (Phillips et al, 1999;Gur et al, 2002b).…”

Section: Introductionmentioning

confidence: 99%

Facial emotion recognition in schizophrenia:When and why does it go awry?

Turetsky

Kohler

Indersmitten

et al. 2007

Schizophrenia Research

215

170

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Objective-Schizophrenia patients demonstrate impaired emotional processing that may be due, in part, to impaired facial emotion recognition. This study examined event-related potential (ERP) responses to emotional faces in schizophrenia patients and controls to determine when, in the temporal processing stream, patient abnormalities occur.Method-16 patients and 16 healthy control participants performed a facial emotion recognition task. Very sad, somewhat sad, neutral, somewhat happy, and very happy faces were each presented for 100 ms. Subjects indicated whether each face was "Happy", "Neutral", or "Sad". Evoked potential data were obtained using a 32-channel EEG system.Results-Controls performed better than patients in recognizing facial emotions. In patients, better recognition of happy faces correlated with less severe negative symptoms. Four ERP components corresponding to the P100, N170, N250, and P300 were identified. Group differences were noted for the N170 "face processing" component that underlies the structural encoding of facial features, but not for the subsequent N250 "affect modulation" component. Higher amplitude of the N170 response to sad faces was correlated with less severe delusional symptoms. Although P300 abnormalities were found, the variance of this component was explained by the earlier N170 response. Conclusion-Patientswith schizophrenia demonstrate abnormalities in early visual encoding of facial features that precedes the ERP response typically associated with facial affect recognition. This suggests that affect recognition deficits, at least for happy and sad discrimination, are secondary Correspondence: Bruce I. Turetsky, M.

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A differential neural response to threatening and non-threatening negative facial expressions in paranoid and non-paranoid schizophrenics

Cited by 273 publications

References 55 publications

Impact of a microRNA MIR137 Susceptibility Variant on Brain Function in People at High Genetic Risk of Schizophrenia or Bipolar Disorder

Impact of a microRNA MIR137 Susceptibility Variant on Brain Function in People at High Genetic Risk of Schizophrenia or Bipolar Disorder

Neural bases for impaired social cognition in schizophrenia and autism spectrum disorders

Facial emotion recognition in schizophrenia:When and why does it go awry?

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