Functional Connectivity Mechanisms Underlying Symptom Reduction Following Lisdexamfetamine Treatment in Binge-Eating Disorder: A Clinical Trial.

Binge-eating disorder Clinical trial Data-driven Default mode network Functional connectivity Lisdexamfetamine

Journal

Biological psychiatry global open science
ISSN: 2667-1743
Titre abrégé: Biol Psychiatry Glob Open Sci
Pays: United States
ID NLM: 9918227369306676

Informations de publication

Date de publication:
Jan 2024
Historique:
received: 25 05 2023
revised: 03 08 2023
accepted: 21 08 2023
medline: 1 2 2024
pubmed: 1 2 2024
entrez: 1 2 2024
Statut: epublish

Résumé

Speculation exists as to whether lisdexamfetamine dimesylate (LDX) acts on the functional connectivity (FC) of brain networks that modulate appetite, reward, or inhibitory control in binge-eating disorder (BED). Better insights into its action may help guide the development of more targeted therapeutics and identify who will benefit most from this medication. Here, we use a comprehensive data-driven approach to investigate the brain FC changes that underlie the therapeutic action of LDX in patients with BED. Forty-six participants with moderate to severe BED received LDX titrated to 50 or 70 mg for an 8-week period. Twenty age-matched healthy control participants were also recruited. Resting-state functional magnetic resonance imaging was used to probe changes in brain FC pre- and post treatment and correlated with change in clinical measures. Ninety-seven percent of trial completers ( FC between networks associated with self-referential processing, executive function, and reward seem to underlie the therapeutic effect of LDX in BED. This suggests that LDX activates change via multiple systems, with most changes in compensatory networks rather than in those characterizing the BED diagnosis.

Sections du résumé

Background UNASSIGNED
Speculation exists as to whether lisdexamfetamine dimesylate (LDX) acts on the functional connectivity (FC) of brain networks that modulate appetite, reward, or inhibitory control in binge-eating disorder (BED). Better insights into its action may help guide the development of more targeted therapeutics and identify who will benefit most from this medication. Here, we use a comprehensive data-driven approach to investigate the brain FC changes that underlie the therapeutic action of LDX in patients with BED.
Methods UNASSIGNED
Forty-six participants with moderate to severe BED received LDX titrated to 50 or 70 mg for an 8-week period. Twenty age-matched healthy control participants were also recruited. Resting-state functional magnetic resonance imaging was used to probe changes in brain FC pre- and post treatment and correlated with change in clinical measures.
Results UNASSIGNED
Ninety-seven percent of trial completers (
Conclusions UNASSIGNED
FC between networks associated with self-referential processing, executive function, and reward seem to underlie the therapeutic effect of LDX in BED. This suggests that LDX activates change via multiple systems, with most changes in compensatory networks rather than in those characterizing the BED diagnosis.

Identifiants

DOI: 10.1016/j.bpsgos.2023.08.016 PMID: 38298797 PMC: PMC10829641
pubmed: 38298797
doi: 10.1016/j.bpsgos.2023.08.016
pii: S2667-1743(23)00106-4
pmc: PMC10829641
doi:

Types de publication

Journal Article

Langues

eng

Pagination

317-325

Informations de copyright

© 2023 The Authors.

Auteurs

Kristi R Griffiths (KR)

Brain Dynamics Centre, Westmead Institute for Medical Research, The University of Sydney, Westmead, New South Wales, Australia.
InsideOut Institute, University of Sydney, Sydney Local Health District, Sydney, New South Wales, Australia.

Isabella A Breukelaar (IA)

Brain Dynamics Centre, Westmead Institute for Medical Research, The University of Sydney, Westmead, New South Wales, Australia.
School of Psychology, University of New South Wales, Sydney, New South Wales, Australia.

Grace Harvie (G)

Brain Dynamics Centre, Westmead Institute for Medical Research, The University of Sydney, Westmead, New South Wales, Australia.

Jenny Yang (J)

Brain Dynamics Centre, Westmead Institute for Medical Research, The University of Sydney, Westmead, New South Wales, Australia.

Sheryl L Foster (SL)

Brain Dynamics Centre, Westmead Institute for Medical Research, The University of Sydney, Westmead, New South Wales, Australia.
Department of Radiology, Westmead Hospital, Sydney, New South Wales, Australia.

Anthony W Harris (AW)

Brain Dynamics Centre, Westmead Institute for Medical Research, The University of Sydney, Westmead, New South Wales, Australia.
Specialty of Psychiatry, Faculty of Medicine and Health, The University of Sydney, Sydney, New South Wales, Australia.

Simon Clarke (S)

Centre for Research into Adolescents' Health, University of Sydney, Sydney, New South Wales, Australia.
Adolescent and Young Adult Medicine, Westmead Hospital, Sydney, New South Wales, Australia.

Phillipa J Hay (PJ)

Translational Health Research Institute, School of Medicine, Western Sydney University, Sydney, New South Wales, Australia.
Mental Health Services, Camden and Campbelltown Hospitals, South Western Sydney Local Health District, Sydney, New South Wales, Australia.

Stephen Touyz (S)

InsideOut Institute, University of Sydney, Sydney Local Health District, Sydney, New South Wales, Australia.
Clinical Psychology Unit, School of Psychology, University of Sydney, Sydney, New South Wales, Australia.

Mayuresh S Korgaonkar (MS)

Brain Dynamics Centre, Westmead Institute for Medical Research, The University of Sydney, Westmead, New South Wales, Australia.

Michael R Kohn (MR)

Brain Dynamics Centre, Westmead Institute for Medical Research, The University of Sydney, Westmead, New South Wales, Australia.
Centre for Research into Adolescents' Health, University of Sydney, Sydney, New South Wales, Australia.
Adolescent and Young Adult Medicine, Westmead Hospital, Sydney, New South Wales, Australia.
Clinical Psychology Unit, School of Psychology, University of Sydney, Sydney, New South Wales, Australia.

Classifications MeSH