Complex functional brain network properties in anorexia nervosa

Arpana Gupta^{1

2

3}, Ravi R Bhatt^{4

5}, Alannah Rivera-Cancel⁶, Rishi Makkar⁴, Philip A Kragel⁷, Thomas Rodriguez⁴, John L Graner⁸, Anita Alaverdyan⁴, Kareem Hamadani⁴, Priten Vora⁴, Bruce Naliboff^{4

9

10}, Jennifer S Labus^{4

9

10}, Kevin S LaBar⁸, Emeran A Mayer^#^{4

9

10

11}, Nancy Zucker^#^{6

8}

Affiliations

¹ G. Oppenheimer Center for Neurobiology of Stress and Resilience, UCLA, Los Angeles, CA, 90095, USA. AGupta@mednet.ucla.edu.
² David Geffen School of Medicine, UCLA, Los Angeles, CA, 90095, USA. AGupta@mednet.ucla.edu.
³ Vatche and Tamar Manoukian Division of Digestive Diseases, UCLA, Los Angeles, CA, 90095, USA. AGupta@mednet.ucla.edu.
⁴ G. Oppenheimer Center for Neurobiology of Stress and Resilience, UCLA, Los Angeles, CA, 90095, USA.
⁵ Imaging Genetics Center, Mark and Mary Stevens Institute for Neuroimaging and Informatics, Keck School of Medicine at USC, University of Southern California, Los Angeles, USA.
⁶ Department of Psychiatry and Behavioral Sciences, Duke University, Durham, USA.
⁷ Department of Psychology, Emory University, Atlanta, USA.
⁸ Department of Psychology and Neuroscience, Duke University, Durham, USA.
⁹ David Geffen School of Medicine, UCLA, Los Angeles, CA, 90095, USA.
¹⁰ Vatche and Tamar Manoukian Division of Digestive Diseases, UCLA, Los Angeles, CA, 90095, USA.
¹¹ Ahmanson-Lovelace Brain Mapping Center, UCLA, Los Angeles, CA, 90095, USA.

^# Contributed equally.

PMID: 35123579
PMCID: PMC8817538
DOI: 10.1186/s40337-022-00534-9

Complex functional brain network properties in anorexia nervosa

Arpana Gupta et al. J Eat Disord. 2022.

. 2022 Feb 5;10(1):13.

doi: 10.1186/s40337-022-00534-9.

Authors

Affiliations

¹ G. Oppenheimer Center for Neurobiology of Stress and Resilience, UCLA, Los Angeles, CA, 90095, USA. AGupta@mednet.ucla.edu.
² David Geffen School of Medicine, UCLA, Los Angeles, CA, 90095, USA. AGupta@mednet.ucla.edu.
³ Vatche and Tamar Manoukian Division of Digestive Diseases, UCLA, Los Angeles, CA, 90095, USA. AGupta@mednet.ucla.edu.
⁴ G. Oppenheimer Center for Neurobiology of Stress and Resilience, UCLA, Los Angeles, CA, 90095, USA.
⁵ Imaging Genetics Center, Mark and Mary Stevens Institute for Neuroimaging and Informatics, Keck School of Medicine at USC, University of Southern California, Los Angeles, USA.
⁶ Department of Psychiatry and Behavioral Sciences, Duke University, Durham, USA.
⁷ Department of Psychology, Emory University, Atlanta, USA.
⁸ Department of Psychology and Neuroscience, Duke University, Durham, USA.
⁹ David Geffen School of Medicine, UCLA, Los Angeles, CA, 90095, USA.
¹⁰ Vatche and Tamar Manoukian Division of Digestive Diseases, UCLA, Los Angeles, CA, 90095, USA.
¹¹ Ahmanson-Lovelace Brain Mapping Center, UCLA, Los Angeles, CA, 90095, USA.

^# Contributed equally.

PMID: 35123579
PMCID: PMC8817538
DOI: 10.1186/s40337-022-00534-9

Abstract

Background: Anorexia nervosa (AN) is a disorder characterized by an incapacitating fear of weight gain and by a disturbance in the way the body is experienced, facets that motivate dangerous weight loss behaviors. Multimodal neuroimaging studies highlight atypical neural activity in brain networks involved in interoceptive awareness and reward processing.

Methods: The current study used resting-state neuroimaging to model the architecture of large-scale functional brain networks and characterize network properties of individual brain regions to clinical measures. Resting-state neuroimaging was conducted in 62 adolescents, 22 (21 female) with a history of AN and 40 (39 female) healthy controls (HCs). Sensorimotor and basal ganglia regions, as part of a 165-region whole-brain network, were investigated. Subject-specific functional brain networks were computed to index centrality. A contrast analysis within the general linear model covarying for age was performed. Correlations between network properties and behavioral measures were conducted (significance q < .05).

Results: Compared to HCs, AN had lower connectivity from sensorimotor regions, and greater connectivity from the left caudate nucleus to the right postcentral gyrus. AN demonstrated lower sensorimotor centrality, but higher basal ganglia centrality. Sensorimotor connectivity dyads and centrality exhibited negative correlations with body dissatisfaction and drive for thinness, two essential features of AN.

Conclusions: These findings suggest that AN is associated with greater communication from the basal ganglia, and lower information propagation in sensorimotor cortices. This is consistent with the clinical presentation of AN, where individuals exhibit patterns of rigid habitual behavior that is not responsive to bodily needs, and seem "disconnected" from their bodies.

Keywords: Anorexia nervosa; Basal ganglia; Functional connectivity; Network metrics; Sensorimotor network.

Plain language summary

Individuals with anorexia nervosa (AN) usually report a fear of gaining weight. They often develop a dislike and distrust of their bodies, feeling that their bodies had somehow let them down. These fears can in turn lead to dangerous weight loss behaviors. Magnetic resonance imaging of the brain is a tool that helps highlight the underlying biological processes associated with AN. In the current study we aim to investigate how the connections in key regions of the brain are related to clinical and behavioral factors associated with AN. We found regions of two main networks were associated with body dissatisfaction and drive for thinness, which are key features of AN. The brain regions involved help explain why patients with AN have characteristics of feeling disconnected from their bodies, having difficulty labeling and regulating emotions, responding to biological needs such as hunger and fatigue, and differentiating experiences that will be rewarding. These results can help guide interventions that will be directed towards helping individuals with AN to better sense, decipher, and act on the various signals being communicated by their body.

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Conflict of interest statement

Each of the authors’ report that no conflicts of interest exist.

Figures

**Fig. 1**
A Differences in functional connectivity between anorexia and healthy controls using whole-brain seed-to-voxel analysis: *SMN* sensorimotor network, BG Basal Ganglia, *DMN* default mode network, *SAL* salience network, *ERN* emotion regulation network, *CAN* central autonomic network, *CEN* central executive network, *Occ* occipital network; *BST* Brainstem Blue: Anorexia < Healthy Controls, Red: Anorexia > Healthy Controls t: t-score. B Differences in functional centrality between anorexia and healthy controls in the sensorimotor and basal ganglia networks: *CaN* caudate nucleus, *SupFG* superior frontal gyrus, *SupFS* superior frontal sulcus, *SubCG* subcentral gyrus and sulcus, *PreCG* precentral gyrus, *PosCG* postcentral gyrus, *PosCS* postcentral sulcus, CS central sulcus, *PaCLS* paracentral lobule and sulcus. Node size represents the degree of centrality of that node based on resting-state functional connectivity. Edge thickness represents the correlation of connectivity between two nodes. Edges between two brain regions in the sensorimotor network are colored in green.

See this image and copyright information in PMC

References

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Complex functional brain network properties in anorexia nervosa

Affiliations

Complex functional brain network properties in anorexia nervosa

Authors

Affiliations

Abstract

Plain language summary

Conflict of interest statement

Figures

References

Grants and funding

LinkOut - more resources

Full Text Sources