Posterior structural brain volumes differ in maltreated youth with and without chronic posttraumatic stress disorder  

Oleh:

Bellis, Michael D. De ; Hooper, Stephen R. ; Chen, Steven D. ; Provenzale, James M. ; Boyd, Brian D. ; Glessner, Christopher E. ; MacFall, James R. ; Payne, Martha E. ; Rybczynski, Robert ; Woolley, Donald P.

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Development and Psychopathology vol. 27 no. 4 (Nov. 2015), page 1555-1576.
Fulltext: DD2115552704022015.pdf (392.34KB)

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Perpustakaan Pusat (Semanggi) Nomor Panggil: DD21 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

Magnetic resonance imaging studies of maltreated children with posttraumatic stress disorder (PTSD) suggest that maltreatment-related PTSD is associated with adverse brain development. Maltreated youth resilient to chronic PTSD were not previously investigated and may elucidate neuromechanisms of the stress diathesis that leads to resilience to chronic PTSD. In this cross-sectional study, anatomical volumetric and corpus callosum diffusion tensor imaging measures were examined using magnetic resonance imaging in maltreated youth with chronic PTSD (N = 38), without PTSD (N = 35), and nonmaltreated participants (n = 59). Groups were sociodemographically similar. Participants underwent assessments for strict inclusion/exclusion criteria and psychopathology. Maltreated youth with PTSD were psychobiologically different from maltreated youth without PTSD and nonmaltreated controls. Maltreated youth with PTSD had smaller posterior cerebral and cerebellar gray matter volumes than did maltreated youth without PTSD and nonmaltreated participants. Cerebral and cerebellar gray matter volumes inversely correlated with PTSD symptoms. Posterior corpus callosum microstructure in pediatric maltreatment-related PTSD differed compared to maltreated youth without PTSD and controls. The group differences remained significant when controlling for psychopathology, numbers of Axis I disorders, and trauma load. Alterations of these posterior brain structures may result from a shared trauma-related mechanism or an inherent vulnerability that mediates the pathway from chronic PTSD to comorbidity.

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