4.7 Article

The interaction effect of early trauma exposure and a diagnosis of panic disorder on cortical thickness

期刊

JOURNAL OF AFFECTIVE DISORDERS
卷 286, 期 -, 页码 259-266

出版社

ELSEVIER
DOI: 10.1016/j.jad.2021.03.008

关键词

Panic disorder; Early trauma; Cortical thickness; Insula; Pars triangularis; Anxiety sensitivity

资金

  1. Basic Science Research Program through the National Research Foundation of Korea (NRF) - Ministry of Science and ICT [NRF-2019M3C7A1032262]
  2. Healthcare AI Convergence Research & Development Program through the National IT Industry Promotion Agency of Korea (NIPA) - Ministry of Science and ICT [S1601-20-1034]
  3. Ministry of Public Safety & Security (MPSS), Republic of Korea [S1601-20-1034] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
  4. National Research Foundation of Korea [2019M3C7A1032262] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

向作者/读者索取更多资源

The study suggests that early trauma exposure may impact brain structures differently based on a diagnosis of panic disorder, and individual variations in brain alterations after early trauma may confer susceptibility to developing panic disorder. Further longitudinal studies are needed to elucidate the neurobiological mechanisms underlying early trauma and psychiatric outcomes.
Background: Early trauma (ET) is a risk factor for adult psychiatric disorders. ET exposure is known to cause structural brain alterations, particularly in the fronto-temporo-limbic circuitry. ET-related effects on brain development may differ based on individual characteristics and cause different psychiatric outcomes. We investigated the interaction effect of ET exposure and panic disorder (PD) on cortical thickness. Methods: Sixty-six participants with PD and 66 healthy controls were enrolled. High-resolution T1-weighted images were acquired, and a whole-brain vertex-based analysis was performed to estimate cortical thickness. The Early Trauma Inventory Self Report-Short Form, Anxiety Sensitivity Inventory-Revised, Panic Disorder Severity Scale, Beck Depression Inventory-II, and Beck Anxiety Inventory were administered. Results: There was a significant interaction between ET exposure and PD on the mean cortical thickness in the bilateral insula and right pars triangularis. An exploratory correlational analysis revealed a positive correlation between the mean cortical thickness in the left insula and severity of anxiety sensitivity to cardiovascular symptoms in participants with PD. Limitations: Our findings may be affected by recall bias because this study is limited by its retrospective crosssectional design. Conclusions: Our findings suggest that ET exposure may affect brain structures differently based on a diagnosis of PD. Furthermore, individual variations in brain alterations after ET may confer trait vulnerability that triggers the development of PD. Future longitudinal studies are warranted to elucidate the neurobiological mechanisms underlying ET and psychiatric outcomes.

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