Increased Gray Matter Density and Functional Connectivity of the Pons in Restless Legs Syndrome.

brainstem gray matter density multivariate pattern analysis restless legs syndrome

Journal

Nature and science of sleep
ISSN: 1179-1608
Titre abrégé: Nat Sci Sleep
Pays: New Zealand
ID NLM: 101537767

Informations de publication

Date de publication:
2020
Historique:
received: 24 11 2019
accepted: 07 03 2020
entrez: 11 4 2020
pubmed: 11 4 2020
medline: 11 4 2020
Statut: epublish

Résumé

Neurophysiological and radiological studies provide accumulating evidence for the involvement of the brainstem in the pathogenesis of restless legs syndrome (RLS). The analysis of the various subregions of the brainstem may help us better understand the pathophysiological mechanisms underlying the disorder. In this study, we investigated the structural and functional changes in the various subregions of the brainstem in RLS patients. The subregional changes in gray matter density and functional connectivity in the brainstem were analyzed in 20 drug-naive idiopathic RLS patients, as well as 18 normal control (NC) subjects for comparison. Correlation analyses and multivariate pattern analyses using linear support vector machine (SVM) were conducted. We found significantly increased gray matter density in two clusters in the pons (designated pons_1 and pons_2) and in one cluster in the midbrain in RLS patients compared with NC subjects. Further functional connectivity analyses revealed significantly decreased functional connectivity between the midbrain and the right middle occipital gyrus, between pons_1 and the right orbital part of the superior frontal gyrus, and between pons_2 and the right parahippocampus in RLS compared with NC. Moreover, the functional connectivity between pons_2 and the right supplementary motor area (SMA) was significantly increased in RLS compared with NC. This change in RLS was marginally correlated with RS_RLS scores in the RLS patients. SVM-based classification showed an AUC of 0.955 using gray matter density of pons_2, and functional connectivity between pons_2 and SMA as features. Collectively, our findings suggest that changes in gray matter density and functional connectivity in the pons may play a pathologic role in RLS. Furthermore, these abnormal changes in the pons might help to discriminate RLS from healthy subjects.

Sections du résumé

BACKGROUND BACKGROUND
Neurophysiological and radiological studies provide accumulating evidence for the involvement of the brainstem in the pathogenesis of restless legs syndrome (RLS). The analysis of the various subregions of the brainstem may help us better understand the pathophysiological mechanisms underlying the disorder. In this study, we investigated the structural and functional changes in the various subregions of the brainstem in RLS patients.
METHODS METHODS
The subregional changes in gray matter density and functional connectivity in the brainstem were analyzed in 20 drug-naive idiopathic RLS patients, as well as 18 normal control (NC) subjects for comparison. Correlation analyses and multivariate pattern analyses using linear support vector machine (SVM) were conducted.
RESULTS RESULTS
We found significantly increased gray matter density in two clusters in the pons (designated pons_1 and pons_2) and in one cluster in the midbrain in RLS patients compared with NC subjects. Further functional connectivity analyses revealed significantly decreased functional connectivity between the midbrain and the right middle occipital gyrus, between pons_1 and the right orbital part of the superior frontal gyrus, and between pons_2 and the right parahippocampus in RLS compared with NC. Moreover, the functional connectivity between pons_2 and the right supplementary motor area (SMA) was significantly increased in RLS compared with NC. This change in RLS was marginally correlated with RS_RLS scores in the RLS patients. SVM-based classification showed an AUC of 0.955 using gray matter density of pons_2, and functional connectivity between pons_2 and SMA as features.
CONCLUSION CONCLUSIONS
Collectively, our findings suggest that changes in gray matter density and functional connectivity in the pons may play a pathologic role in RLS. Furthermore, these abnormal changes in the pons might help to discriminate RLS from healthy subjects.

Identifiants

pubmed: 32273784
doi: 10.2147/NSS.S239852
pii: 239852
pmc: PMC7102916
doi:

Types de publication

Journal Article

Langues

eng

Pagination

221-230

Informations de copyright

© 2020 Xu et al.

Déclaration de conflit d'intérêts

None of the authors have any conflict of interest to disclose.

Références

Brain. 2005 Apr;128(Pt 4):906-17
pubmed: 15728657
J Gerontol A Biol Sci Med Sci. 2010 Feb;65(2):167-73
pubmed: 19914971
Sleep Med. 2008 Jul;9(5):500-5
pubmed: 17869573
Sleep Med. 2009 Dec;10(10):1155-7
pubmed: 19307154
Mov Disord. 2010 Nov 15;25(15):2641-8
pubmed: 20836134
Mov Disord. 2009 Jan 15;24(1):77-84
pubmed: 18816657
J Neurol. 2010 Dec;257(12):1979-85
pubmed: 20635185
J Cereb Blood Flow Metab. 2012 Apr;32(4):654-62
pubmed: 22234337
Neuroimage. 2015 Jun;113:184-95
pubmed: 25776214
Sleep Med. 2006 Jan;7(1):25-30
pubmed: 16198145
Mov Disord. 2003 Nov;18(11):1403-5
pubmed: 14639696
Sleep Med. 2017 Mar;31:39-48
pubmed: 27838239
Behav Neurol. 2013;27(1):57-64
pubmed: 23187144
J Sleep Res. 2019 Jun 25;:e12890
pubmed: 31237744
J Neuroimaging. 2012 Jan;22(1):28-32
pubmed: 21091816
Nihon Rinsho. 2015 Jun;73(6):916-23
pubmed: 26065120
Front Neurol. 2018 Dec 17;9:1098
pubmed: 30619055
Brain Behav. 2015 Sep;5(9):e00327
pubmed: 26442748
Mov Disord. 2007 Sep 15;22(12):1751-6
pubmed: 17566123
Clin Imaging. 2015 Jan-Feb;39(1):20-5
pubmed: 25176196
Sleep Med. 2003 Mar;4(2):101-19
pubmed: 14592341
Parkinsonism Relat Disord. 2004 Oct;10(7):429-31
pubmed: 15465401
Sleep Med. 2019 Oct;62:34-42
pubmed: 31539846
J Neurol. 2005 Jan;252(1):67-71
pubmed: 15654556
Sleep Med. 2014 Aug;15(8):860-73
pubmed: 25023924
Eur J Neurol. 2012 Jul;19(7):1045-9
pubmed: 22175823
Phys Ther. 2009 Mar;89(3):267-82
pubmed: 19168711
Suppl Clin Neurophysiol. 2006;58:52-67
pubmed: 16623322
Lancet Neurol. 2018 Nov;17(11):994-1005
pubmed: 30244828
J Rheumatol. 1998 Nov;25(11):2270-5
pubmed: 9818676
J Clin Neurosci. 2012 May;19(5):702-5
pubmed: 22364890
J Neurosci. 2005 Aug 10;25(32):7333-41
pubmed: 16093383
J Neurol Sci. 1994 Sep;125(2):194-7
pubmed: 7807167
Neurology. 2001 Jan 23;56(2):263-5
pubmed: 11160969
Neurology. 2010 Feb 9;74(6):513-8
pubmed: 20142619
J Neurol. 2010 Mar;257(3):344-8
pubmed: 19768657
Sleep Med. 2007 Dec;9(1):22-6
pubmed: 17512782
Sleep Med. 2012 Oct;13(9):1202-4
pubmed: 22995627
Sleep. 2009 Aug;32(8):1069-76
pubmed: 19725258
CNS Drugs. 2010 Feb;24(2):89-98
pubmed: 20088617
Sleep Med. 2011 Jun;12(6):614-9
pubmed: 21570342
Neuroimage. 2005 Feb 15;24(4):1242-7
pubmed: 15670702
Neurology. 2000 Apr 25;54(8):1609-16
pubmed: 10762502
Ann Neurol. 1997 May;41(5):639-45
pubmed: 9153526
Sleep Med Rev. 2019 Jun;45:70-87
pubmed: 30965199
Sleep. 2009 May;32(5):589-97
pubmed: 19480225
Nat Rev Neurol. 2010 Jun;6(6):337-46
pubmed: 20531433
Pain. 2006 Jul;123(1-2):169-78
pubmed: 16616418
Brain. 2012 Dec;135(Pt 12):3712-20
pubmed: 23183234
Sleep. 2016 Feb 01;39(2):423-8
pubmed: 26446110
ScientificWorldJournal. 2011 Mar 22;11:736-41
pubmed: 21442151
Cough. 2013 Mar 06;9(1):7
pubmed: 23497672
Sleep Med. 2014 Oct;15(10):1225-30
pubmed: 25129262
Mov Disord. 2008 Jul 15;23(9):1250-5
pubmed: 18464282
Brain. 2006 Aug;129(Pt 8):2017-28
pubmed: 16816393

Auteurs

Zhexue Xu (Z)

Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing 100053, People's Republic of China.
Beijing Key Laboratory of Neuromodulation, Beijing 100053, People's Republic of China.

Tao Han (T)

Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing 100053, People's Republic of China.
Beijing Key Laboratory of Neuromodulation, Beijing 100053, People's Republic of China.

Tian Li (T)

Institute of Biomedical and Health Engineering, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen 518055, People's Republic of China.

Xiaodong Zhang (X)

Institute of Biomedical and Health Engineering, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen 518055, People's Republic of China.

Zhaoyang Huang (Z)

Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing 100053, People's Republic of China.
Beijing Key Laboratory of Neuromodulation, Beijing 100053, People's Republic of China.

Shuqin Zhan (S)

Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing 100053, People's Republic of China.
Beijing Key Laboratory of Neuromodulation, Beijing 100053, People's Republic of China.

Chunyan Liu (C)

Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing 100053, People's Republic of China.
Beijing Key Laboratory of Neuromodulation, Beijing 100053, People's Republic of China.

Jinping Xu (J)

Institute of Biomedical and Health Engineering, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen 518055, People's Republic of China.

Yuping Wang (Y)

Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing 100053, People's Republic of China.
Beijing Key Laboratory of Neuromodulation, Beijing 100053, People's Republic of China.

Classifications MeSH