This application is a 5-year cross-sectional investigation with a one-year prospective follow-up to non-invasively examine the psychobiology of childhood posttraumatic stress disorder (PTSD) secondary to sexual abuse. In cross-sectional studies, we reported that clinically referred maltreated children with PTSD had elevated 24-hour urinary catecholamine and free cortisol levels and smaller intracranial and cerebral volumes, smaller midsaggital areas of the corpus callosum. and larger ventricles compared to non-abused controls. PTSD trauma for the majority of these children was sexual abuse. Earlier age of onset of abuse, longer duration of abuse, and greater PTSD symptoms each were associated with more extreme difference from normals on these measures. Animal studies suggest that elevated levels of catecholamines and cortisol during development may lead to adverse brain development. Our pilot study did not address to what extent our results were PTSD specific or the result of abuse. We will examine the diagnosis and severity of PTSD on outcomes of biological stress system regulation and brain maturation. We will study 3 groups of 70 children (35 males/35 females), aged 6 to 12 years: children with PTSD secondary to sexual abuse, sexually abused children without PTSD, and non-traumatized age and sociodemographically comparable controls. Biological stress system regulation will be assessed by 24-hour urinary catecholamine and free cortisol levels. Brain maturation will be assessed by: magnetic resonance spectroscopy-based brain N-acetylaspartate concentrations, which reflect neuronal integrity, magnetic resonance imaging-based brain morphometry (cerebral, amygdala/hippocampal volumes and corpus callosum area), and cognitive function. This study includes a cross-sectional component at entry (Time-01) and a one-year follow-up (Time-02). Study entry for abused subjects is within 3 months of abuse disclosure. Time-01 and -02 assessments measure known risk factors for the development of PTSD.
Specific aims are to determine the relationship between sexual abuse with PTSD and without PTSD and these outcomes at Time-01 and to determine the one-year effects of sexual abuse with PTSD and sexual abuse without PTSD on these same children's biological stress systems and neuropsychological function. Secondary aims are: to identify the psychobiological predictors of the persistence of PTSD and resiliency to PTSD at the one-year period after abuse disclosure (Time-02). We hypothesize that sexually abused children with PTSD will show evidence of alterations in biological stress systems and brain maturation at Time-01 and Time-02. We further hypothesize that certain risk factors at Time-01 (e.g. age of onset of abuse, adverse life events, and biological measures) will predict the persistence of PTSD at Time-02.
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