11:00am - 11:10amIndices of connectivity and psychopathology in psychotic disorders
Armida Mucci1, Kathryn Rieger2, Giulia Maria Giordano1, Giorgio Di Lorenzo3, Dean Salisbury4
1University of Campania Luigi Vanvitelli, Italy; 2Translational Research Center, University Hospital of Psychiatry, University of Bern, Switzerland; 3Department of Systems Medicine, University of Rome “Tor Vergata”, Italy; 4Clinical Neurophysiology Research Laboratory, Western Psychiatric institute and Clinic, Department of Psychiatry, University of Pittsburgh School of Medicine, PA, USA
It has been long suggested that the different symptom domains of schizophrenia are best explained in terms of aberrant connectivity within distributed brain networks.
Electrophysiological and brain imaging studies might contribute to disentangle the neurobiological basis of different psychopathological dimensions which might be related to disconnection within different networks.
The aim of our symposium will be to summarize recent electrophysiological and brain imaging findings of altered connectivity in psychotic disorders and their association with psychopathological domains.
11:10am - 11:25amBrain electrical microstate and the positive symptom domain in schizophrenia
Kathryn Rieger, Laura Diaz, Thomas Koenig
University Hospital of Psychiatry, Switzerland
We will report brain electrical microstate correlates of positive symptoms and discuss the involved pathophysiological mechanisms. This report will in particular be based on a recent meta-analysis conducted across the available literature, novel data we have obtained from at-risk patients, and existing literature on the fMRI BOLD correlates of particular microstate classes. The overall picture from this analysis points at a dysbalance between processes that integrate and evaluate representations of information from the external world with representations of internal states.
11:25am - 11:40amNeurobiological bases of negative symptom domains in schizophrenia: a resting-EEG microstates study
Giulia Maria Giordano1, Thomas Koenig2, Armida Mucci1, Annarita Vignapiano1, Antonella Amodio1, Giorgio di Lorenzo3, Cinzia Niolu3, Mario Altamura4, Antonello Bellomo4, Silvana Galderisi1
1University of Campania "Luigi Vanvitelli", Italy; 2University Hospital of Psychiatry, University of Bern; 3Department of Systems Medicine, University of Rome “Tor Vergata”, Italy; 4Dipartimento di Medicina Clinica e Sperimentale, Universita di Foggia
Negative symptoms represent a key aspect of schizophrenia, with a worse outcome and a poor response to pharmacological treatment. They cluster into two domains: “avolition”, which includes apathy, anhedonia and asociality, and “expressive deficit”, which includes blunted affect and alogia.
The aim of this study was to investigate the different neurobiological correlates of negative symptoms domains using brain electrical microstates (MS), which reflect global, subsecond patterns of functional connectivity.
Resting EEGs were recorded in 142 schizophrenia patients (SCZ) and in 64 healthy controls (HC), recruited within the add-on EEG study of the Italian Network for Research on Psychoses. Four microstates classes (MS-A to MS-D) were quantified in terms of relative time contribution, duration and occurrence. We tested group differences on MS parameters and the relationships with negative symptom domains, assessed using the Brief Negative Symptoms Scale (BNSS).
SCZ, in comparison to HC, showed increased contribution (p=0.009) and duration (p=0.016) of MS-C.
As regard to negative symptoms, the total score of the BNSS was positively correlated with the contribution of MS-A (r= 0.19, p<0.03). Only avolition (r=0.22, p<0.01) and not expressive deficit (r=0.12, p=0.15) was correlated with contribution of MS-A. Within the avolition domain, anticipatory anhedonia (r=0.20, p=0.02), apathy (r=0.20, p=0.02) and asociality (r=0.25, p=0.003), but not consummatory anhedonia (r=0.13, p=0.13), were positively correlated with MS-A.
Our results support different neurobiological underpinnings of negative symptom domains and suggest the idea that only anticipatory anhedonia and not consummatory anhedonia shares common pathophysiological mechanisms with avolition.
11:40am - 11:55amResting-state EEG functional connectivity and expressive deficit in Schizophrenia
Giorgio Di Lorenzo1, Armida Mucci2, Annarita Vignapiano2, Giulia Maria Giordano2, Cinzia Niolu1, Mario Altamura3, Antonello Belomo3, Silvana Galderisi2
1University of Rome Tor Vergata, Italy; 2University of Campania "Luigi Vanvitelli", Italy; 3Dipartimento di Medicina Clinica e Sperimentale, Universita di Foggia
<p>We investigated relations between resting-state EEG Source Functional Connectivity (EEG-SFC) and Expressive Deficit (ED) and Avolition (AV) measured with BNSS, in subjects with Schizophrenia (SCZ).</p>
<p>Out of 97 chronic, stabilized SCZ recorded, we selected 25 in upper (HIGH-ED) and 24 in the lower (LOW-ED) quartile of BNSS-ED and 27 in upper (HIGH-AV) and 24 in the lower (LOW-AV) quartile of BNSS-AV.</p>
<p>Respect to LOW-ED, HIGH-ED showed significant increased alpha connectivity in fronto-cingulate, para-hippocampal and insular inter-hemispheric regions. No significant difference emerged between HIGH-AV and LOW-AV in the source connectivity.</p>
<p>Subgrouping SCZ according to negative symptom severity reveals heterogeneous patterns of resting-state EEG-SFC.</p>
11:55am - 12:10pmTranscallosal auditory cortex white matter connectivity and auditory verbal hallucinations in emerging psychosis
Dean F Salisbury
University of Pittsburgh School of Medicine, United States of America
Auditory cortices show pathological activation during auditory verbal hallucinations (AVH) in schizophrenia, and reduced cortical gray matter volumes at first hospitalization that worsen with disease course. Here we explored the role of interhemispheric transcallosal connectivity in AVH in 31 first episode schizophrenia-spectrum psychosis (FESz). Spearman’s rank-order correlation revealed a relationship between reduced generalized functional anisotropy and increased AVH (rho = -.43, p =.016). This finding suggests that impaired structural connectivity between left and right hemisphere auditory cortices may play a role in AVH and the emergence of psychosis.
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