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Differential Neural Correlates of Dimensions of Negative Symptoms in Schizophrenia During Social-emotional Appraisal and Effects of Treatment

Published online by Cambridge University Press:  23 March 2020

A. Aleman*
Affiliation:
Department of Neuroscience, Umc, Groningen, The Netherlands

Abstract

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Factor analyses of large datasets have established two dimensions of negative symptoms: expressive deficits and a motivation. This distinction is of relevance as the dimensions differ in their cognitive and clinical correlates (e.g. with regard to functional outcome). Using functional MRI, we examined the neural correlates of the two negative symptom dimensions with brain activation during social-emotional evaluation. Patients with schizophrenia (n = 38) and healthy controls (n = 20) performed the Wall of Faces task during fMRI, which measures emotional ambiguity in a social context by presenting an array of faces with varying degrees of consistency in emotional expressions. More specifically, appraisal of facial expressions under uncertainty. We found severity of expressive deficits to be negatively correlated with activation in thalamic, prefrontal, precentral, parietal and temporal brain areas during emotional ambiguity (appraisal of facial expressions in an equivocal versus an unequivocal condition). No association was found for a motivation with these neural correlates, in contrast to a previous fMRI study in which we found a motivation to be associated with neural correlates of executive (planning) performance. We also evaluated the effects of medication and neurostimulation (rTMS treatment over the lateral prefrontal cortex) on activation during the social–emotional ambiguity task. The medication comparison concerned an RCT of aripiprazole versus risperidone. Compared to risperidone, aripiprazole showed differential involvement of frontotemporal and frontostriatal circuits in social-emotional ambiguity. We conclude that deconstruction of negative symptoms into more homogeneous components and investigating underlying neurocognitive mechanisms can potentially shed more light on their nature and may ultimately yield clues for targeted treatment.

Disclosure of interest

AA received speaker fees from Lundbeck.

Type
Symposium: Social cognition in schizophrenia: pathophysiology, functional implications and treatment options
Copyright
Copyright © European Psychiatric Association 2017
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