Subcallosal Cingulate Structural Connectivity Differs in Responders and Nonresponders to Electroconvulsive Therapy.


Journal

Biological psychiatry. Cognitive neuroscience and neuroimaging
ISSN: 2451-9030
Titre abrégé: Biol Psychiatry Cogn Neurosci Neuroimaging
Pays: United States
ID NLM: 101671285

Informations de publication

Date de publication:
01 2021
Historique:
received: 01 05 2020
revised: 21 05 2020
accepted: 24 05 2020
pubmed: 4 8 2020
medline: 4 6 2021
entrez: 4 8 2020
Statut: ppublish

Résumé

Subcallosal cingulate (SCC) activity is associated with treatment response in major depressive disorder (MDD). Using electroconvulsive therapy (ECT) as a treatment model in this exploratory study, we addressed whether pretreatment SCC structural connectivity with corticolimbic-striatal circuitry relates to therapeutic outcome and whether these connectivity patterns change with treatment. Diffusion magnetic resonance imaging scans were acquired in 43 patients with MDD (mean [SD] age = 41 [13] years; men/women: 18/25) before and within 1 week of completing an ECT index series and in 31 healthy control subjects scanned twice (mean [SD] age = 38 [11] years; men/women: 17/18). Probabilistic tractography from subject-specific anatomically defined SCC seed regions to the ventral striatum (VS), anterior cingulate cortex (ACC), and bilateral medial prefrontal cortex (mPFC) was used to estimate structural connectivity in the target network. SCC-mPFC connectivity was lower in responders (>50% symptom improvement) than nonresponders both before (p < .014) (difference 37%-96% left and right hemispheres) and after (p = .023) (difference 100% right hemisphere) treatment. SCC-mPFC connectivity in responders was also decreased compared with control subjects both at baseline (p = .012) and after ECT (p = .006), whereas nonresponders had SCC-right mPFC connectivity similar to that of control subjects. Subjects with MDD also showed decreased SCC-ACC connectivity compared with control subjects (baseline: p < .003, after ECT: p = .001), although SCC-ACC connectivity did not distinguish responders from nonresponders. Bilateral SCC-VS connectivity decreased (11%) with ECT (p = .021) regardless of treatment response. While SCC-ACC connectivity may be a hallmark of MDD compared with control subjects, lower pretreatment SCC-mPFC connectivity in ECT responders (compared with nonresponders and control subjects) suggests that connectivity in this pathway may serve as a potential biomarker of therapeutic outcome and be relevant for treatment selection.

Sections du résumé

BACKGROUND
Subcallosal cingulate (SCC) activity is associated with treatment response in major depressive disorder (MDD). Using electroconvulsive therapy (ECT) as a treatment model in this exploratory study, we addressed whether pretreatment SCC structural connectivity with corticolimbic-striatal circuitry relates to therapeutic outcome and whether these connectivity patterns change with treatment.
METHODS
Diffusion magnetic resonance imaging scans were acquired in 43 patients with MDD (mean [SD] age = 41 [13] years; men/women: 18/25) before and within 1 week of completing an ECT index series and in 31 healthy control subjects scanned twice (mean [SD] age = 38 [11] years; men/women: 17/18). Probabilistic tractography from subject-specific anatomically defined SCC seed regions to the ventral striatum (VS), anterior cingulate cortex (ACC), and bilateral medial prefrontal cortex (mPFC) was used to estimate structural connectivity in the target network.
RESULTS
SCC-mPFC connectivity was lower in responders (>50% symptom improvement) than nonresponders both before (p < .014) (difference 37%-96% left and right hemispheres) and after (p = .023) (difference 100% right hemisphere) treatment. SCC-mPFC connectivity in responders was also decreased compared with control subjects both at baseline (p = .012) and after ECT (p = .006), whereas nonresponders had SCC-right mPFC connectivity similar to that of control subjects. Subjects with MDD also showed decreased SCC-ACC connectivity compared with control subjects (baseline: p < .003, after ECT: p = .001), although SCC-ACC connectivity did not distinguish responders from nonresponders. Bilateral SCC-VS connectivity decreased (11%) with ECT (p = .021) regardless of treatment response.
CONCLUSIONS
While SCC-ACC connectivity may be a hallmark of MDD compared with control subjects, lower pretreatment SCC-mPFC connectivity in ECT responders (compared with nonresponders and control subjects) suggests that connectivity in this pathway may serve as a potential biomarker of therapeutic outcome and be relevant for treatment selection.

Identifiants

pubmed: 32741703
pii: S2451-9022(20)30134-8
doi: 10.1016/j.bpsc.2020.05.010
pii:
doi:

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

10-19

Subventions

Organisme : NIMH NIH HHS
ID : R01 MH092301
Pays : United States
Organisme : NIMH NIH HHS
ID : U01 MH110008
Pays : United States
Organisme : NIMH NIH HHS
ID : K24 MH102743
Pays : United States

Informations de copyright

Copyright © 2020 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.

Auteurs

Evangelia Tsolaki (E)

Department of Neurosurgery, University of California, Los Angeles, Los Angeles, California. Electronic address: etsolaki@mednet.ucla.edu.

Katherine L Narr (KL)

Department of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, Los Angeles, California; Ahmanson-Lovelace Brain Mapping Center, Department of Neurology, University of California, Los Angeles, Los Angeles, California.

Randall Espinoza (R)

Department of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, Los Angeles, California.

Benjamin Wade (B)

Department of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, Los Angeles, California; Ahmanson-Lovelace Brain Mapping Center, Department of Neurology, University of California, Los Angeles, Los Angeles, California.

Gerhard Hellemann (G)

Department of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, Los Angeles, California.

Antoni Kubicki (A)

Department of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, Los Angeles, California; Ahmanson-Lovelace Brain Mapping Center, Department of Neurology, University of California, Los Angeles, Los Angeles, California.

Megha Vasavada (M)

Department of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, Los Angeles, California; Ahmanson-Lovelace Brain Mapping Center, Department of Neurology, University of California, Los Angeles, Los Angeles, California.

Stephanie Njau (S)

Department of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, Los Angeles, California; Ahmanson-Lovelace Brain Mapping Center, Department of Neurology, University of California, Los Angeles, Los Angeles, California.

Nader Pouratian (N)

Department of Neurosurgery, University of California, Los Angeles, Los Angeles, California.

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Classifications MeSH