Abstract
We constructed a novel design integrating the administration of a clinical self-assessment scale with simultaneous acquisition of functional Magnetic Resonance Imaging (fMRI), aiming at cross-validation between psychopathology evaluation and neuroimaging techniques. We hypothesized that areas demonstrating differential activation in two groups of patients (the first group exhibiting paranoid delusions in the context of paranoid schizophrenia—SCH—and second group with a depressive episode in the context of major depressive disorder or bipolar disorder—DEP) will have distinct connectivity patterns and structural differences. Fifty-one patients with SCH (n = 25) or DEP (n = 26) were scanned with three different MRI sequences: a structural and two functional sequences—resting-state and task-related fMRI (the stimuli represent items from a paranoid-depressive self-evaluation scale). While no significant differences were found in gray matter volumes, we were able to discriminate between the two clinical entities by identifying two significant clusters of activations in the SCH group—the left Precuneus (PreCu) extending to the left Posterior Cingulate Cortex (PCC) and the right Angular Gyrus (AG). Additionally, the effective connectivity of the middle frontal gyrus (MFG), a part of the Dorsolateral Prefrontal Cortex (DLPFC) to the Anterior Insula (AI), demonstrated a significant difference between the two groups with inhibitory connection demonstrated only in SCH. The observed activations of PreCu, PCC, and AG (involved in the Default Mode Network DMN) might be indirect evidence of the inhibitory connection from the DLPFC to AI, interfering with the balancing function of the insula as the dynamic switch in the DMN. The findings of our current study might suggest that the connectivity from DLPFC to the anterior insula can be interpreted as evidence for the presence of an aberrant network that leads to behavioral abnormalities, the manifestation of which depends on the direction of influence. The reduced effective connectivity from the AI to the DLPFC is manifested as depressive symptoms, and the inhibitory effect from the DLPFC to the AI is reflected in the paranoid symptoms of schizophrenia.
Highlights
Mental disorders constitute one of the major sources of economic burden in modern society in addition to the stigmatization of mental illness
The results of the present study on schizophrenic and depressed patients can be summarized as follows: (i) there were no significant structural differences between the groups in terms of gray matter volumes on a whole-brain voxel-by-voxel comparison; (ii) the SCH group demonstrated significantly more activation in the left precuneus and left posterior cingulate gyrus, as well as the right superior parietal lobule and angular gyrus, during the processing of the paranoid items of the von Zerssen scale when contrasted with the depression items; (iii) the connection from the middle frontal gyrus to the anterior insula was the only significantly different in the direct comparison between the groups, several other connections at group level seemed to be different as well
Structural changes as evident in GM volume reductions of different brain regions have been found in schizophrenia and in depression when compared to healthy controls [28,29,30]
Summary
Mental disorders constitute one of the major sources of economic burden in modern society in addition to the stigmatization of mental illness. Schizophrenia (SCH), in particular, are accountable for a significant percentage of the disability-adjusted life years as a criterion for economic and social burden worldwide [1]. These disorders, especially the treatment-resistant forms, are associated with highly decreased quality of life and a significant increase in comorbidities and suicide risk [2,3]. Several studies have provided evidence for existing shared genetic correlations between psychiatric conditions such as psychosis, depression, autism spectrum disorder, and bipolar disorder [4,5]. Nervous System (CNS) discovered by MRI, such as grey-matter volume reduction in the anterior cingulate cortex (ACC), can define a genetic vulnerability to psychosis [6].
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