Elevated body weight modulates subcortical volume change and associated clinical response following electroconvulsive therapy.
Journal
Journal of psychiatry & neuroscience : JPN
ISSN: 1488-2434
Titre abrégé: J Psychiatry Neurosci
Pays: Canada
ID NLM: 9107859
Informations de publication
Date de publication:
05 07 2021
05 07 2021
Historique:
entrez:
5
7
2021
pubmed:
6
7
2021
medline:
19
1
2022
Statut:
epublish
Résumé
Obesity is a frequent somatic comorbidity of major depression, and it has been associated with worse clinical outcomes and brain structural abnormalities. Converging evidence suggests that electroconvulsive therapy (ECT) induces both clinical improvements and increased subcortical grey matter volume in patients with depression. However, it remains unknown whether increased body weight modulates the clinical response and structural neuroplasticity that occur with ECT. To address this question, we conducted a longitudinal investigation of structural MRI data from the Global ECT-MRI Research Collaboration (GEMRIC) in 223 patients who were experiencing a major depressive episode (10 scanning sites). Structural MRI data were acquired before and after ECT, and we assessed change in subcortical grey matter volume using FreeSurfer and Quarc. Higher body mass index (BMI) was associated with a significantly lower increase in subcortical grey matter volume following ECT. We observed significant negative associations between BMI and change in subcortical grey matter volume, with pronounced effects in the thalamus and putamen, where obese participants showed increases in grey matter volume that were 43.3% and 49.6%, respectively, of the increases found in participants with normal weight. As well, BMI significantly moderated the association between subcortical grey matter volume change and clinical response to ECT. We observed no significant association between BMI and clinical response to ECT. Because only baseline BMI values were available, we were unable to study BMI changes during ECT and their potential association with clinical and grey matter volume change. Future studies should take into account the relevance of body weight as a modulator of structural neuroplasticity during ECT treatment and aim to further explore the functional relevance of this novel finding.
Sections du résumé
Background
Obesity is a frequent somatic comorbidity of major depression, and it has been associated with worse clinical outcomes and brain structural abnormalities. Converging evidence suggests that electroconvulsive therapy (ECT) induces both clinical improvements and increased subcortical grey matter volume in patients with depression. However, it remains unknown whether increased body weight modulates the clinical response and structural neuroplasticity that occur with ECT.
Methods
To address this question, we conducted a longitudinal investigation of structural MRI data from the Global ECT-MRI Research Collaboration (GEMRIC) in 223 patients who were experiencing a major depressive episode (10 scanning sites). Structural MRI data were acquired before and after ECT, and we assessed change in subcortical grey matter volume using FreeSurfer and Quarc.
Results
Higher body mass index (BMI) was associated with a significantly lower increase in subcortical grey matter volume following ECT. We observed significant negative associations between BMI and change in subcortical grey matter volume, with pronounced effects in the thalamus and putamen, where obese participants showed increases in grey matter volume that were 43.3% and 49.6%, respectively, of the increases found in participants with normal weight. As well, BMI significantly moderated the association between subcortical grey matter volume change and clinical response to ECT. We observed no significant association between BMI and clinical response to ECT.
Limitations
Because only baseline BMI values were available, we were unable to study BMI changes during ECT and their potential association with clinical and grey matter volume change.
Conclusion
Future studies should take into account the relevance of body weight as a modulator of structural neuroplasticity during ECT treatment and aim to further explore the functional relevance of this novel finding.
Identifiants
pubmed: 34223741
doi: 10.1503/jpn.200176
pmc: PMC8410473
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
E418-E426Subventions
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 : U01 MH111826
Pays : United States
Informations de copyright
© 2021 CMA Joule Inc. or its licensors.
Déclaration de conflit d'intérêts
A. Dale reports that he was a founder of and holds equity in CorTechs Labs, Inc., and serves on its scientific advisory board; he is a member of the scientific advisory boards of Human Longevity, Inc., the Mohn Medical Imaging and Visualization Centre; he receives funding through research grants from GE Healthcare to UCSD. The terms of these arrangements have been reviewed by and approved by the University of California, San Diego in accordance with its conflict of interest policies. No other competing interests declared.
Références
Neurology. 2019 Feb 5;92(6):e594-e600
pubmed: 30626649
Biol Psychiatry. 2020 Mar 1;87(5):451-461
pubmed: 31561859
Psychoneuroendocrinology. 2015 Jan;51:219-26
pubmed: 25462895
Elife. 2019 Oct 23;8:
pubmed: 31644424
Brain Stimul. 2019 Mar - Apr;12(2):335-343
pubmed: 30554869
Neuropsychopharmacology. 2016 Sep;41(10):2481-91
pubmed: 27067127
Mol Psychiatry. 2020 May 28;:
pubmed: 32467648
Acta Psychiatr Scand. 2018 Sep;138(3):180-195
pubmed: 29707778
Am J Geriatr Psychiatry. 2007 Oct;15(10):899-905
pubmed: 17911366
Neuroscience. 2013 Nov 12;252:109-17
pubmed: 23933215
Biol Psychiatry. 2016 Feb 15;79(4):282-92
pubmed: 25842202
Arch Gen Psychiatry. 2010 Mar;67(3):220-9
pubmed: 20194822
J Neurosci. 2011 Mar 23;31(12):4360-6
pubmed: 21430137
Neuroimage Clin. 2017 Feb 14;14:422-432
pubmed: 28275543
Neuroimage. 2006 Apr 1;30(2):436-43
pubmed: 16300968
J ECT. 2014 Jun;30(2):143-51
pubmed: 24810772
Brain Stimul. 2019 Sep - Oct;12(5):1135-1142
pubmed: 31176607
PLoS One. 2014 Mar 12;9(3):e91251
pubmed: 24622163
Mol Psychiatry. 2020 Nov;25(11):2860-2872
pubmed: 30940904
Mol Psychiatry. 2017 Jun;22(6):900-909
pubmed: 27137745
Acta Psychiatr Scand. 2016 Feb;133(2):154-164
pubmed: 26138003
Biol Psychiatry. 2007 Aug 15;62(4):321-6
pubmed: 17241618
Diabetes Care. 2013 Feb;36(2):443-9
pubmed: 23069842
Neuroimage. 2015 Nov 15;122:149-57
pubmed: 26256530
PLoS One. 2016 Feb 10;11(2):e0148361
pubmed: 26863521
JAMA Psychiatry. 2016 Jun 1;73(6):557-64
pubmed: 27145449
Mol Psychiatry. 2020 Jul;25(7):1559-1568
pubmed: 30867562
Hum Brain Mapp. 2012 Nov;33(11):2586-602
pubmed: 21830259
Nat Rev Neurosci. 2012 Jul;13(7):465-77
pubmed: 22678511
Lancet. 2003 Mar 8;361(9360):799-808
pubmed: 12642045
Mol Psychiatry. 2019 Jan;24(1):18-33
pubmed: 29453413
Hum Brain Mapp. 2014 Jan;35(1):75-88
pubmed: 23008165
Biol Psychiatry. 2018 Oct 15;84(8):574-581
pubmed: 30006199
Brain Behav Immun. 2014 Nov;42:10-21
pubmed: 24727365
Brain Behav Immun. 2016 Mar;53:39-48
pubmed: 26546831
Lancet Diabetes Endocrinol. 2018 Mar;6(3):223-236
pubmed: 28919064
Mol Psychiatry. 2016 Jun;21(6):806-12
pubmed: 26122586
Alzheimers Dement. 2018 May;14(5):601-609
pubmed: 29169013
Bipolar Disord. 2019 Feb;21(1):50-60
pubmed: 30422375
Br J Psychiatry. 2019 Mar;214(3):159-167
pubmed: 30442205
Obesity (Silver Spring). 2015 Oct;23(10):2066-74
pubmed: 26347385
Psychol Med. 2020 Jan;50(2):187-209
pubmed: 31858931
Transl Psychiatry. 2020 Apr 20;10(1):108
pubmed: 32312958
Neuropsychopharmacology. 2015 Jan;40(2):463-71
pubmed: 25074636
JAMA Psychiatry. 2017 Dec 1;74(12):1214-1225
pubmed: 29049554
Sci Rep. 2019 Sep 9;9(1):12885
pubmed: 31501448
Hum Brain Mapp. 2012 Sep;33(9):2204-10
pubmed: 22887828
Neuron. 2002 Jan 31;33(3):341-55
pubmed: 11832223
J Neuropsychiatry Clin Neurosci. 2019 Spring;31(2):152-158
pubmed: 30458664
Mol Psychiatry. 2021 Apr;26(4):1399-1408
pubmed: 31467393
Hum Brain Mapp. 2013 Jul;34(7):1737-46
pubmed: 22419507