Hostname: page-component-848d4c4894-jbqgn Total loading time: 0 Render date: 2024-06-23T08:30:53.986Z Has data issue: false hasContentIssue false

Impaired connectivity in amygdala pathways may explain disorganization symptoms of patients with first-episode schizophrenia

Published online by Cambridge University Press:  24 June 2014

P Das
Affiliation:
Neuroscience Institute of Schizophrenia and Allied Disorders (NISAD); Brain Dynamics Centre
D Alexander
Affiliation:
Brain Resource Company
P Boord
Affiliation:
Brain Dynamics Centre
K Brown
Affiliation:
Brain Dynamics Centre
G Flynn
Affiliation:
Liverpool Hospital, Early Psychosis Intervention Program
C Galletly
Affiliation:
University of Adelaide
E Gordon
Affiliation:
Brain Resource Company
A Harris
Affiliation:
Brain Dynamics Centre The University of Sydney, Australia
T Whitford
Affiliation:
Brain Dynamics Centre
L Williams
Affiliation:
Brain Dynamics Centre
W Wong
Affiliation:
Liverpool Hospital, Early Psychosis Intervention Program
Rights & Permissions [Opens in a new window]

Abstract

Type
Abstracts from ‘Brainwaves’— The Australasian Society for Psychiatric Research Annual Meeting 2006, 6–8 December, Sydney, Australia
Copyright
Copyright © 2006 Blackwell Munksgaard

Background:

Our integrative neuroscience model of first-episode schizophrenia (FES) highlights the lack of coordinated neural activity required for effective processing of salient signals of emotion. Aim of this study was to determine whether altered connectivity of frontolimbic networks underlies impairments in coordinated processing of emotion and associated clinical profile.

Methods:

Functional magnetic resonance imaging (fMRI) scans were acquired in 14 patients with FES and 14 matched healthy control subjects during the pseudorandom presentation of fearful and neutral facial expression stimuli. Faces were presented under both overt (conscious) and covert (nonconscious) conditions shown to engage indirect cortical and direct brainstem pathways to the amygdala, respectively. A random-effects model with the following regions of interest (ROIs) was used: amygdala, brainstem, thalamus, visual cortex and the medial prefrontal cortex (MPFC). Following group comparisons, we used psychophysi-ological interaction analysis to examine coupling of amygdala with other ROIs. We used the effect size of differences in coupling in regression analyses to predict patients' clinical profile assessed with the PANSS.

Results:

Patients with FES showed a differential pattern of amygdala interaction with the nodes of direct and indirect pathways and also with the MPFC compared with controls. A greater impairment in these couplings, particularly during conscious processing of fear faces, predicted a greater severity in the conceptual and behavioural disorganization measured by PANSS.

Conclusion:

These findings indicate that break down in amygdala pathways may affect coordinated neural activity required for effective processing of salient signals of emotion and may lead to a disruption of the usual emotional and cognitive associations such as incongruent affect.