Abstract
Contemporary theories propose that dysregulation of emotional perception is involved in the aetiology of psychosis. 298 healthy adolescents were assessed at age 14- and 19-years using fMRI while performing a facial emotion task. Psychotic-like experiences (PLEs) were assessed with the CAPE-42 questionnaire at age 19. The high PLEs group at age 19 years exhibited an enhanced response in right insular cortex and decreased response in right prefrontal, right parahippocampal and left striatal regions; also, a gradient of decreasing response to emotional faces with age, from 14 to 19 years, in the right parahippocampal region and left insular cortical area. The right insula demonstrated an increasing response to emotional faces with increasing age in the low PLEs group, and a decreasing response over time in the high PLEs group. The change in parahippocampal/amygdala and insula responses during the perception of emotional faces in adolescents with high PLEs between the ages of 14 and 19 suggests a potential ‘aberrant’ neurodevelopmental trajectory for critical limbic areas. Our findings emphasize the role of the frontal and limbic areas in the aetiology of psychotic symptoms, in subjects without the illness phenotype and the confounds introduced by antipsychotic medication.
Highlights
Www.nature.com/scientificreports regions; a gradient of decreasing response to emotional faces with age, from 14 to 19 years, in the right parahippocampal region and left insular cortical area
Five regions of interest (ROIs) based on previous studies of facial emotion processing in psychosis and Ultra-High Risk (UHR) for psychosis[15,16] were used; the prefrontal cortices, the temporal cortices, the limbic brain and the striatum were included for factorial analysis
There was a main effect of time on Affective Go-NoGo Task (AGN) Total Omissions for both positive
Summary
Www.nature.com/scientificreports regions; a gradient of decreasing response to emotional faces with age, from 14 to 19 years, in the right parahippocampal region and left insular cortical area. A developmental model of psychosis describes transitory symptoms, such as PLEs and attenuated psychotic symptoms (psychosis proneness) becoming abnormally resilient (persistence) and subsequently clinically relevant (symptoms of clinical psychosis and impairment) This model is in line with the contemporary view that psychotic symptoms are not “all-or-nothing” pathological phenomena but rather fall within a spectrum ranging from normal, transient PLEs to pervasive psychotic symptoms, conceptualised as the continuum model of psychosis[2]. Aberrant activation of the amygdalae and related regions including the parahippocampal cortex during processing of emotional stimuli was reflected in an inability to appropriately utilise and contextualise social cues This deficit would naturally lead to the development of inappropriate suspicion, persecutory beliefs, with further impairment of interpersonal functioning[12]. The insular cortices, caudate[13] and the right parahippocampal gyrus[14] demonstrate attenuated activation during facial emotion processing in patients with schizophrenia
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