Neural activity during response inhibition associated with improvement of dysphoric symptoms of PTSD after trauma-focused psychotherapy-an EEG-fMRI study.


Journal

Translational psychiatry
ISSN: 2158-3188
Titre abrégé: Transl Psychiatry
Pays: United States
ID NLM: 101562664

Informations de publication

Date de publication:
14 04 2021
Historique:
received: 28 05 2020
accepted: 29 03 2021
revised: 10 03 2021
entrez: 15 4 2021
pubmed: 16 4 2021
medline: 29 6 2021
Statut: epublish

Résumé

Although trauma-focused cognitive behavioural therapy (TF-CBT) is the frontline treatment for posttraumatic stress disorder (PTSD), up to one half of patients do not respond optimally to this treatment. Inhibitory functions are important for successful management of PTSD, yet there is a dearth of knowledge regarding the extent to which neural mechanisms unpinning response inhibition are associated with TF-CBT response. Treatment-seeking PTSD patients (n = 40) were assessed during a response inhibition task (the Go/No-Go task) while undergoing functional magnetic imaging (fMRI) and event-related potentials (ERP) in separate sessions. PTSD symptom severity was assessed with the Clinician-Administered PTSD Scale, before undergoing nine sessions of TF-CBT. They were then reassessed post-treatment to estimate reduction in fear and dysphoric symptoms of PTSD. Although neural responses during the inhibitory task did not predict overall symptom change, reduced activation in the left precuneus and the right superior parietal cortex predicted greater improvement in dysphoric symptoms. ERP responses during response inhibition indicated that lower P3 peak latency predicted greater reduction of dysphoric symptoms. There were no significant predictors of changes of fear symptoms. These findings indicate that neural activity associated with response inhibition can act as a predictive biomarker of TF-CBT response for PTSD symptoms. This pattern of findings underscores the importance of delineating the role of biomarkers to predict remission of subtypes of PTSD.

Identifiants

pubmed: 33854050
doi: 10.1038/s41398-021-01340-8
pii: 10.1038/s41398-021-01340-8
pmc: PMC8046805
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

218

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Auteurs

Richard A Bryant (RA)

School of Psychology, University of New South Wales, Sydney, NSW, Australia. r.bryant@unsw.edu.au.
Brain Dynamics Centre, Westmead Institute for Medical Research, University of Sydney, Sydney, NSW, Australia. r.bryant@unsw.edu.au.

Thomas Williamson (T)

School of Psychology, University of New South Wales, Sydney, NSW, Australia.
Brain Dynamics Centre, Westmead Institute for Medical Research, University of Sydney, Sydney, NSW, Australia.

May Erlinger (M)

Brain Dynamics Centre, Westmead Institute for Medical Research, University of Sydney, Sydney, NSW, Australia.

Kim L Felmingham (KL)

School of Psychological Sciences, University of Melbourne, Melbourne, VIC, Australia.

Gin Malhi (G)

Department of Psychiatry, University of Sydney, Sydney, NSW, Australia.

Mark Hinton (M)

Phoenix Australia, University of Melbourne, Melbourne, VIC, Australia.

Leanne Williams (L)

Department of Psychiatry and Behavioral Sciences, Stanford University, Stanford, CA, USA.
Sierra-Pacific Mental Illness Research, Education, and Clinical Center (MIRECC) VA Palo Alto Health Care System, Palo Alto, CA, USA.

Mayuresh S Korgaonkar (MS)

Brain Dynamics Centre, Westmead Institute for Medical Research, University of Sydney, Sydney, NSW, Australia.
School of Health Sciences, Faculty of Medicine and Health, University of Sydney, Sydney, NSW, Australia.

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