The effect of trauma upon anyone can have a long lasting impact on their brain. For children, trauma can have a permanent impact on their developing brain, yet they may never meet the criteria for PTSD (Teicher, Anderson, Polcari, Anderson, & Navalta, 2002). For children however, traumatic stress can come from multiple and/or chronic and prolonged, developmentally adverse traumatic events during early childhood development (van der Kolk 2005). This has led to a new classification, Developmental Trauma (DT). Areas of the brain involved in the stress response include the amygdala, hippocampus, and prefrontal cortex, which also play a role in memory (Bremner 2006). Research by Sapolsky found stress can alter plasticity of the limbic system, not only affecting hormone secretion, but also how the hippocampus and amygdala work together to form memories about the stressor (2003). Comparing maltreated groups to control groups, Teicher, Samson, Anderson, and Ohashi also found connectivity issues as well in the left anterior cingulate, right occipital pole, left temporal pole, and right medial frontal gyrus (2016). Regions of decreased connectivity were found in areas important to emotional regulation, attention and social cognition, while areas with increased connectivity seemed to occur in areas of self-regulation (Teicher, Samson, Anderson, Ohashi, 2016).
EEG/QEEG research on developmental trauma is quite scant. One study found that abused children had higher left hemisphere coherence and a reversed asymmetry as well as a slower rate of decay of left hemisphere coherence over electrode distance suggesting deficit in left cortical differentiation (Ito, Teicher, Glod, & Ackerman, 1998). Our study aims to study the impact of repeated developmental trauma on brain function and connectivity. We hypothesize adults that experienced DT will show significantly different findings than those that did not have such a history. Further, we anticipate that susceptible regions may include those near the anterior cingulate left frontal temporal and limbic regions and right posterior regions involved in social engagement.
We are in the midst of collecting QEEG data (19 and 64 channels) on 30 survivors of DT and a comparison group. The groups will be compared for differences in EEG power, coherence and connectivity. Using EEGLAB and MVGC (multivariate granger causality toolbox) we will measure scalp and source measures for comparison as indicated above. Source comparisons will be made insuring finer spatial localization of the network components while minimizing signal processing confounds produced by broad volume conduction from neural sources to the scalp electrodes (Coben, Mohammad-Rezazadeh, & Cannon 2014). Source derived connectivity measures including Granger Causality and partial directed coherence will be applied. Group based comparisons of these metrics will be displayed and case examples will be used as well for illustrative purposes. The implications of these findings for understanding DT and its treatment will be discussed.
