22.2 WHAT DO BRAIN STRUCTURES ASSOCIATED WITH EXTINCTION LEARNING HAVE TO DO WITH POSTTRAUMATIC STRESS DISORDER AND LATER ADDICTIONS?

• Published in: Journal of the American Academy of Child and Adolescent Psychiatry Vol. 55; no. 10; p. S292
• Main Author: DeBellis, Michael, MD
• Format: Journal Article
• Language: English
• Published: Baltimore Elsevier BV 01.10.2016
• Subjects: Abused children; Adolescents; Alcohol use; Amygdala; Anatomy; Brain; Brain structure; Cerebellum; Child & adolescent psychiatry; Cognition; Cognitive ability; Comorbidity; Cortex; Cortex (cingulate); Cortex (frontal); Cortex (occipital); Cortex (parietal); Drinking behavior; Extinction; Extinction behavior; Hippocampus; Learning; Neuroimaging; Pediatrics; Post traumatic stress disorder; Posttraumatic Stress Disorder; Prefrontal cortex; Psychiatry; Psychological distress; Risk assessment; Scientific Concepts; Substantia alba; Substantia grisea; Trauma
• ISSN: 0890-8567; 1527-5418
• DOI: 10.1016/j.jaac.2016.07.245

Objectives: Maltreated youth are at higher risk for PTSD and subsequent addictions. Methods: Two unique studies will be presented. In one study, maltreated youth with PTSD (n = 38) and without PTSD (n = 35) and nonmaltreated youth (n 59) underwent anatomical brain imaging (age range 6-16 years) for total gray and white matter volumes and structures associated with extinction learning [orbital frontal cortex (OFC), also called ventral medial prefrontal cortex (vmPFC), anterior cingulate, amygdala, and hippocampus]. In addition, cross-sectional anatomical total gray and white matter cortical volume data from the National Consortium on Alcohol and NeuroDevelopment in Adolescence study (NCANDA) compared 617 low- to no-drinking adolescents without trauma history to 57 low- to no-drinking adolescents (age range 12-21 years) whose trauma history and response to distress lasted more than 1 month. Results: Maltreated youth with PTSD had greater axis I comorbidity and demonstrated smaller OFC (P < 0.05) and less posterior and cerebellar gray matter volumes (P < 0.005) than maltreated youth without PTSD and nonmaltreated subjects. In the NCANDA sample group, decreased gray matter volumes were seen in parietal and cingulate cortex (P < 0.05), and decreased surface area was seen in frontal, parietal, occipital, and cingulate cortex in noand/or low-drinking NCANDA group with trauma (P < 0.05). Conclusions: Cortical deficits are seen very early in pediatric PTSD and before known abnormalities are seen in adult PTSD. Along with the findings from NCANDA in which subjects with early trauma and symptoms of PTSD showed similar findings, it is possible that anatomical differences in key structures associated with cognitive control and extinction learning may represent a shared risk mechanism for PTSD. These findings may also represent a shared risk mechanism for both PTSD and addictions and be related to either trauma or early factors that predate early trauma.