Multimodal Magnetic Resonance Imaging Depicts Widespread and Subregion Specific Anomalies in the Thalamus of Early-Psychosis and Chronic Schizophrenia Patients.
MRI
early-psychosis
microstructure
nuclei
schizophrenia
thalamus
Journal
Schizophrenia bulletin
ISSN: 1745-1701
Titre abrégé: Schizophr Bull
Pays: United States
ID NLM: 0236760
Informations de publication
Date de publication:
03 01 2023
03 01 2023
Historique:
pubmed:
7
9
2022
medline:
6
1
2023
entrez:
6
9
2022
Statut:
ppublish
Résumé
Although the thalamus has a central role in schizophrenia pathophysiology, contributing to sensory, cognitive, and sleep alterations, the nature and dynamics of the alterations occurring within this structure remain largely elusive. Using a multimodal magnetic resonance imaging (MRI) approach, we examined whether anomalies: (1) differ across thalamic subregions/nuclei, (2) are already present in the early phase of psychosis (EP), and (3) worsen in chronic schizophrenia (SCHZ). T1-weighted and diffusion-weighted images were analyzed to estimate gray matter concentration (GMC) and microstructural parameters obtained from the spherical mean technique (intra-neurite volume fraction [VFINTRA)], intra-neurite diffusivity [DIFFINTRA], extra-neurite mean diffusivity [MDEXTRA], extra-neurite transversal diffusivity [TDEXTRA]) within 7 thalamic subregions. Compared to age-matched controls, the thalamus of EP patients displays previously unreported widespread microstructural alterations (VFINTRA decrease, TDEXTRA increase) that are associated with similar alterations in the whole brain white matter, suggesting altered integrity of white matter fiber tracts in the thalamus. In both patient groups, we also observed more localized and heterogenous changes (either GMC decrease, MDEXTRA increase, or DIFFINTRA decrease) in mediodorsal, posterior, and ventral anterior parts of the thalamus in both patient groups, suggesting that the nature of the alterations varies across subregions. GMC and DIFFINTRA in the whole thalamus correlate with global functioning, while DIFFINTRA in the subregion encompassing the medial pulvinar is significantly associated with negative symptoms in SCHZ. Our data reveals both widespread and more localized thalamic anomalies that are already present in the early phase of psychosis.
Sections du résumé
BACKGROUND AND HYPOTHESIS
Although the thalamus has a central role in schizophrenia pathophysiology, contributing to sensory, cognitive, and sleep alterations, the nature and dynamics of the alterations occurring within this structure remain largely elusive. Using a multimodal magnetic resonance imaging (MRI) approach, we examined whether anomalies: (1) differ across thalamic subregions/nuclei, (2) are already present in the early phase of psychosis (EP), and (3) worsen in chronic schizophrenia (SCHZ).
STUDY DESIGN
T1-weighted and diffusion-weighted images were analyzed to estimate gray matter concentration (GMC) and microstructural parameters obtained from the spherical mean technique (intra-neurite volume fraction [VFINTRA)], intra-neurite diffusivity [DIFFINTRA], extra-neurite mean diffusivity [MDEXTRA], extra-neurite transversal diffusivity [TDEXTRA]) within 7 thalamic subregions.
RESULTS
Compared to age-matched controls, the thalamus of EP patients displays previously unreported widespread microstructural alterations (VFINTRA decrease, TDEXTRA increase) that are associated with similar alterations in the whole brain white matter, suggesting altered integrity of white matter fiber tracts in the thalamus. In both patient groups, we also observed more localized and heterogenous changes (either GMC decrease, MDEXTRA increase, or DIFFINTRA decrease) in mediodorsal, posterior, and ventral anterior parts of the thalamus in both patient groups, suggesting that the nature of the alterations varies across subregions. GMC and DIFFINTRA in the whole thalamus correlate with global functioning, while DIFFINTRA in the subregion encompassing the medial pulvinar is significantly associated with negative symptoms in SCHZ.
CONCLUSION
Our data reveals both widespread and more localized thalamic anomalies that are already present in the early phase of psychosis.
Identifiants
pubmed: 36065156
pii: 6692485
doi: 10.1093/schbul/sbac113
pmc: PMC9810016
doi:
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
196-207Informations de copyright
© The Author(s) 2022. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center. All rights reserved. For permissions, please email: journals.permissions@oup.com.
Références
J Neurosci. 2007 Dec 12;27(50):13835-42
pubmed: 18077695
Early Interv Psychiatry. 2013 Aug;7(3):322-8
pubmed: 23445318
Schizophr Res. 2019 Aug;210:270-277
pubmed: 30630706
IEEE Trans Med Imaging. 1991;10(3):395-407
pubmed: 18222842
J Anat. 2019 Sep;235(3):507-520
pubmed: 30657169
Schizophr Res. 2017 Feb;180:28-35
pubmed: 27567291
Lancet. 1999 Jan 2;353(9146):30-3
pubmed: 10023948
Arch Gen Psychiatry. 2003 Oct;60(10):983-91
pubmed: 14557143
Schizophr Bull. 1987;13(2):261-76
pubmed: 3616518
Biol Psychiatry. 2019 Jan 1;85(1):70-78
pubmed: 29961564
Neuroimage. 2009 Oct 1;47(4):1163-71
pubmed: 19375511
JAMA Psychiatry. 2015 Sep;72(9):882-91
pubmed: 26267151
Schizophr Res. 2020 Dec;226:147-157
pubmed: 31147286
Psychiatry Res. 2014 Jan 30;221(1):69-77
pubmed: 24239093
Indian J Psychol Med. 2013 Jan;35(1):34-8
pubmed: 23833340
Schizophr Res. 2003 Apr 1;60(2-3):141-55
pubmed: 12591578
Am J Psychiatry. 2020 Dec 1;177(12):1159-1167
pubmed: 32911995
Wiley Interdiscip Rev Dev Biol. 2019 Sep;8(5):e345
pubmed: 31034163
Neuroimage. 2016 Oct 1;139:346-359
pubmed: 27282476
Neuroimage. 2017 Nov 1;161:149-170
pubmed: 28826946
Neuroreport. 2008 Mar 5;19(4):399-403
pubmed: 18287935
Schizophr Res. 2016 May;173(1-2):23-9
pubmed: 27012899
Schizophr Res. 2004 Aug 1;69(2-3):237-53
pubmed: 15469196
Eur Neuropsychopharmacol. 2014 May;24(5):645-92
pubmed: 24820238
Mol Psychiatry. 2016 Jun;21(6):823-30
pubmed: 26416546
Hum Brain Mapp. 2020 Oct 1;41(14):4041-4061
pubmed: 33448519
NPJ Schizophr. 2016 Sep 28;2:16033
pubmed: 27738647
Neuroimage. 2019 Jan 1;184:801-812
pubmed: 30267859
Mol Psychiatry. 2018 Oct;23(10):2057-2065
pubmed: 29180672
Neuroimage. 2012 Aug 15;62(2):782-90
pubmed: 21979382
Mol Psychiatry. 2018 May;23(5):1261-1269
pubmed: 29038599
Mol Neuropsychiatry. 2015 Dec;1(4):191-200
pubmed: 27606313
Neuroimage. 2019 Nov 15;202:116137
pubmed: 31473352
Biol Psychiatry. 2001 May 15;49(10):811-23
pubmed: 11343678
Biol Psychiatry. 2004 Jul 1;56(1):41-5
pubmed: 15219471
Front Neuroinform. 2014 Apr 28;8:44
pubmed: 24817849
Biol Psychiatry. 1999 May 1;45(9):1099-119
pubmed: 10331102
Brain Imaging Behav. 2019 Apr;13(2):472-481
pubmed: 29667043
Biol Psychiatry. 2010 Feb 1;67(3):255-62
pubmed: 19897178
Front Hum Neurosci. 2015 Jan 09;8:1027
pubmed: 25620923
Acta Neuropathol. 2009 Apr;117(4):347-68
pubmed: 18604544
Nat Commun. 2018 Sep 21;9(1):3836
pubmed: 30242220
Schizophr Res. 2013 Dec;151(1-3):148-53
pubmed: 24094679
Brain Imaging Behav. 2018 Jun;12(3):640-652
pubmed: 28444556
Aust N Z J Psychiatry. 2005 Nov-Dec;39(11-12):964-71
pubmed: 16343296
PLoS One. 2017 Sep 25;12(9):e0184661
pubmed: 28945803
Neuroimage. 2012 Jul 16;61(4):1000-16
pubmed: 22484410
J Psychiatr Res. 2010 Dec;44(16):1176-89
pubmed: 20471030
Eur Arch Psychiatry Clin Neurosci. 1999;249(4):174-9
pubmed: 10449592
Hum Brain Mapp. 2009 Apr;30(4):1236-45
pubmed: 18570200
Schizophr Bull. 2016 May;42(3):723-31
pubmed: 26598740
Can J Psychiatry. 1997 Feb;42(1):27-33
pubmed: 9040920
Br J Psychiatry. 2012 Jan;200(1):30-6
pubmed: 22116979
Neurology. 2015 Feb 17;84(7):738-47
pubmed: 25609762
Neuron. 2002 Jan 31;33(3):341-55
pubmed: 11832223
Neuroimage. 2006 Aug 1;32(1):16-22
pubmed: 16626974
Neuroimage Clin. 2017 Mar 06;14:622-628
pubmed: 28348953
Neuroimage. 2012 Mar;60(1):340-52
pubmed: 22178809
Neuron. 2012 May 24;74(4):691-705
pubmed: 22632727
Mol Psychiatry. 2021 Dec;26(12):7709-7718
pubmed: 34462574
Neurosci Biobehav Rev. 2015 Jul;54:57-75
pubmed: 25616183