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Schizophr Bull. 2018 Apr 17. doi: 10.1093/schbul/sby047. [Epub ahead of print]

Multimodal Brain Changes in First-Episode Mania: A Voxel-Based Morphometry, Functional Magnetic Resonance Imaging, and Connectivity Study.

Author information

1
Barcelona Bipolar Disorders Unit, Hospital Clinic, University of Barcelona, IDIBAPS, CIBERSAM, Barcelona, Catalonia, Spain.
2
Department of Psychology, School of Arts and Social Sciences, City University London, London, UK.
3
Department of Neuroimaging, Institute of Psychiatry, Psychology and Neuroscience, King's College London, UK.
4
FIDMAG Germanes Hospitalàries Research Foundation, Benito Menni Complex Assistencial en Salut Mental, CIBERSAM, Barcelona, Catalonia, Spain.
5
Department of Psychiatry, University of Milan, Milan, Italy.
6
Department of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, NY.

Abstract

Background:

Brain structural and functional changes in bipolar disorder (BD) are well-established findings, but it is uncertain whether these changes are already present in first episode mania (FEM).

Methods:

We compared 31 FEM subjects, with 31 healthy individuals matched for age, sex, and premorbid IQ. Whole-brain voxel-wise morphometry, functional magnetic resonance imaging during the n-back task, and a functional connectivity analysis were performed.

Results:

There were no volumetric differences between the 2 groups. During the 2-back task, FEM patients did not perform differently from controls and activated similar regions, but they showed less deactivation in the ventromedial prefrontal cortex (vmPFC), the anterior hub of the default mode network (DMN). They showed preserved functional connectivity between the vmPFC and other regions of the DMN, but increased connectivity with the superior frontal gyrus.

Conclusions:

The absence of volumetric changes in FEM patients suggests that these changes could be related to progression of the illness. On the other hand, the failure of deactivation of the anterior hub of the DMN is present from the onset of the illness and may represent a core pathophysiological feature of BD.

PMID:
29672741
DOI:
10.1093/schbul/sby047

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