Can traumatic stress alter the brain? Understanding the implications of early trauma on brain development and learning.

BACKGROUND: Youth who experience traumatic stress and develop post-traumatic symptoms secrete higher levels of the glucocorticoid cortisol than youth with no trauma history. Animal research suggests that excess corticosterone secretion can lead to neurotoxicity in areas of the brain rich in glucocorticoid receptors such as the hippocampus and the prefrontal cortex (PFC). These two areas of the brain are involved in memory processing and executive function, both critical functions of learning. METHODS: In this article, we summarize findings presented at the National Summit for Stress and the Brain conducted at Johns Hopkins University's Department of Public Health in April 2011. The presentation highlighted structural and functional imaging findings in the hippocampus and PFC of youth with post-traumatic stress symptoms (PTSS). RESULTS: Youth with PTSS have higher levels of cortisol. Prebedtime cortisol levels predict decreases in hippocampal volume longitudinally. Cortisol levels are negatively correlated with volume in the PFC. Functional imaging studies demonstrate reduced hippocampal and PFC activities on tasks of memory and executive function in youth with PTSS when compared with control subjects. CONCLUSIONS: Effective interventions for youth with PTSS should target improved function of frontolimbic networks. Treatment outcome research using these potential markers can help develop more focused interventions that target the impaired learning of vulnerable youth experiencing traumatic stress.

Ethnic differences in viral dominance patterns in patients with hepatitis B virus and hepatitis C virus dual infection.

UNLABELLED: Studies of hepatitis B virus (HBV)/hepatitis C virus (HCV) dual infection are limited. Most are small, conducted outside the United States, and compare dual infection with HCV monoinfection. The goal of this study was to characterize HBV/HCV dual infection in a large multiethnic, matched, case-control study of dual-infected and HBV-monoinfected patients at two United States centers. Using an International Classification of Disease Version 9 electronic query and chart review, we identified 115 HBV/HCV dual-infected patients with serial HBV DNA, HCV RNA, and alanine aminotransferase (ALT) levels. As a control, 115 HBV-monoinfected patients were chosen randomly and matched with cases by age ±10 years, sex, Asian versus non-Asian ethnicity, and study site. Both groups had similar sex, ethnic, and age distributions (68% male, 83% Asian, age 52 ± 14 years). The median follow-up times were 33 and 38 months for the dual-infected and monoinfected groups, respectively. More monoinfected patients received HBV antiviral therapy than dual-infected patients (43% versus 24%; P = 0.002). No significant difference was detected between the proportion of monoinfected versus dual-infected patients with ALT above 40 U/L at presentation or during follow-up. Dual infection patients exhibited very little HBV/HCV codominance at baseline and throughout follow-up: patients had either HBV viremia with low or absent HCV RNA or detectable HCV RNA with low or absent HBV DNA. Asian ethnicity was predictive of HBV dominance after adjusting for sex, age, and baseline ALT elevation (odds ratio 7.35; P = 0.01). CONCLUSION: HBV/HCV dual-infected and HBV-monoinfected patients had similar clinical characteristics. Asian ethnicity is a major independent predictor of HBV-dominant disease, and HCV dominance with undetectable HBV DNA is more common in non-Asian individuals. Larger studies are needed to further characterize the natural history of HBV/HCV dual infection in Asian and non-Asian individuals.