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PTSD REMISSION AFTER PROLONGED EXPOSURE TREATMENT IS ASSOCIATED WITH ANTERIOR CINGULATE CORTEX THINNING AND VOLUME REDUCTION
Author(s) -
Helpman Liat,
Papini Santiago,
Chhetry Binod T.,
Shvil Erel,
Rubin Mikael,
Sullivan Gregory M.,
Markowitz John C.,
Mann J. John,
Neria Yuval
Publication year - 2016
Publication title -
depression and anxiety
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.634
H-Index - 129
eISSN - 1520-6394
pISSN - 1091-4269
DOI - 10.1002/da.22471
Subject(s) - anterior cingulate cortex , magnetic resonance imaging , confounding , medicine , psychology , psychiatry , cognition , radiology
Background Brain structures underlying posttraumatic stress disorder (PTSD) have been a focus of imaging studies, but associations between treatment outcome and alterations in brain structures remain largely unexamined. We longitudinally examined the relation of structural changes in the rostral anterior cingulate cortex (rACC), a previously identified key region in the PTSD fear network, to outcome of prolonged exposure (PE) treatment. Method The sample included 78 adults (53 women): 41 patients with PTSD and 37 trauma‐exposed healthy volunteers (TE‐HCs). Patients underwent a 10‐week course of PE treatment and completed pre‐ and posttreatment assessments and magnetic resonance imaging (MRI) structural scans. TE‐HCs also underwent assessment and MRI at baseline and 10 weeks later. PE remitters ( n  = 11), nonremitters ( n  = 14), and TE‐HCs, were compared at baseline on demographic and clinical characteristics and ACC structure. Remitters, nonremitters, and TE‐HCs were compared for pre‐ to posttreatment clinical and structural ACC change, controlling for potential confounding variables. Results There were no baseline differences in structure between PTSD and TE‐HCs or remitters and nonremitters. Following treatment, PTSD remitters exhibited cortical thinning and volume decrease in the left rACC compared with PTSD nonremitters and TE‐HCs. Conclusions These results, while in need of replication, suggest that PE treatment for PTSD, by extinguishing maladaptive trauma associations, may promote synaptic plasticity and structure change in rACC. Future research should explore possible underlying mechanisms.

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