Hyperactivation of the Frontal Control Network Revealed by Symptom Provocation in Obsessive-Compulsive Disorder Using EEG Microstate and sLORETA Analyses.


Journal

Neuropsychobiology
ISSN: 1423-0224
Titre abrégé: Neuropsychobiology
Pays: Switzerland
ID NLM: 7512895

Informations de publication

Date de publication:
2019
Historique:
received: 12 03 2018
accepted: 28 06 2018
pubmed: 25 9 2018
medline: 16 4 2019
entrez: 25 9 2018
Statut: ppublish

Résumé

The aim of this study was to investigate the changes of brain electric field induced by symptom provocation in patients with obsessive-compulsive disorder (OCD) in comparison to healthy controls in the resting state. For this purpose, EEG recordings in conditions of initial rest, clean control, symptom provocation by imaginal exposure, and final rest were used for computing spatiotemporal activity characteristics based on microstate segmentation. Within-group comparisons were significant for the symptom provocation condition: OCD showed high global field power (GFP) and transition rates into a medial frontal microstate, whereas healthy controls showed high frequency of occurrence and high percent of dwelling time for a medial occipitoparietal microstate. Between-group comparisons demonstrated significantly lower GFP and dwelling time for the medial occipitoparietal microstate in OCD in several conditions including initial rest and symptom provocation. In addition, OCD compared to healthy controls showed significant instability of the medial occipitoparietal microstate, with high preference for transitions into the medial frontal microstate. In conclusion, during rest and symptom provocation, OCD patients make preferential use of a medial frontal brain network, with concomitant reduction of use of a medial occipitoparietal network, as shown by dwelling times, explained variance, and dynamic transition rates. These findings support the idea of a possible biological marker for OCD, which might correspond to pathological hyperactivation of the frontal control network.

Identifiants

pubmed: 30248667
pii: 000491719
doi: 10.1159/000491719
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

176-185

Informations de copyright

© 2018 S. Karger AG, Basel.

Auteurs

Masafumi Yoshimura (M)

Department of Neuropsychiatry, Kansai Medical University, Osaka, Japan, yoshimum@takii.kmu.ac.jp.

Roberto D Pascual-Marqui (RD)

Department of Neuropsychiatry, Kansai Medical University, Osaka, Japan.
The KEY Institute for Brain-Mind Research, University Hospital of Psychiatry, Zurich, Switzerland.

Keiichiro Nishida (K)

Department of Neuropsychiatry, Kansai Medical University, Osaka, Japan.

Yuichi Kitaura (Y)

Department of Neuropsychiatry, Kansai Medical University, Osaka, Japan.

Hiroshi Mii (H)

Department of Neuropsychiatry, Kansai Medical University, Osaka, Japan.
Setagawa Hospital, Otsu, Japan.

Yukiko Saito (Y)

Department of Neuropsychiatry, Kansai Medical University, Osaka, Japan.

Shunichiro Ikeda (S)

Department of Neuropsychiatry, Kansai Medical University, Osaka, Japan.
Department of Psychiatric Neurophysiology, University Hospital of Psychiatry, Bern, Switzerland.

Koji Katsura (K)

Department of Neuropsychiatry, Kansai Medical University, Osaka, Japan.

Satsuki Ueda (S)

Department of Neuropsychiatry, Kansai Medical University, Osaka, Japan.

Shota Minami (S)

Department of Neuropsychiatry, Kansai Medical University, Osaka, Japan.

Toshiaki Isotani (T)

Department of Neuropsychiatry, Kansai Medical University, Osaka, Japan.
Department of Brain-Mind Research, Shikoku University Faculty of Nursing, Tokushima, Japan.

Toshihiko Kinoshita (T)

Department of Neuropsychiatry, Kansai Medical University, Osaka, Japan.

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