The purpose of this study was to identify correlates hypothetically linked to PTSS in maltreated children, using the developmental traumatology model. Using hierarchical regression, low SES, the General Maltreatment, and Sexual Abuse Factors were independent correlates of PTSD symptoms. In addition to the variables in the main developmental traumatology model, poorer visual memory was significantly associated with more PTSD symptoms.
Hippocampal volumes did not predict PTSD symptoms in these models. In adults, most studies show smaller hippocampal volumes in individuals with PTSD from a variety of traumas occurring at different developmental time periods (Kitayama, Vaccarino, Kutner, Weiss, & Bremner, 2005
). Smaller hippocampal volumes are seen in most adults with PTSD secondary to child abuse (Bremner et al., 2003
) and combat (Freeman, Cardwell, Karson, & Komoroski, 1998
). However, smaller hippocampal volumes are not seen in children with histories of maltreatment related PTSD (De Bellis, Hall, Boring, Frustaci, & Moritz, 2001
; De Bellis, Keshavan, et al., 1999
; De Bellis et al., 2002
) or who have threshold and subthreshold PTSD (Carrion, Weems, Eliez et al., 2001
). Hippocampal volume differences were not seen in survivors of the Nazi Holocaust with and without PTSD, and who were children during the Holocaust, although memory deficits were present (Gollier et al., 2005
). It is possible that we were able to demonstrate hippocampal dysfunction (i.e., poorer visual memory) prior to any evidence of smaller MRI measures of the hippocampus for our young population. Smaller hippocampal volumes may be related to a latent effect that manifests in adolescence (Carrion et al., 2007
) or adulthood.
Our finding of poorer visual memory may reflect dysfunction of the hippocampus, but not reduced volume. The finding may also reflect dysfunction of other brain regions, such as the right hemisphere (Fjell et al., 2005
), left parahippocampal area and the left lingual gyrus (Schmidt et al., 2007
) and parietal and prefrontal cortices (Yago & Ishai, 2006
). In a developmental study of visual memory of younger and older adults, right cortical volume and hippocampal volume were independent predictors of memory function, leading the authors to conclude that memory function is not uniquely related to the hippocampus (Fjell et al., 2005
). Moreover, child maltreatment is a risk for addictions, a frequent lifetime comorbid event in the adults described in most of this existing literature (De Bellis, 2002
). It is possible that comorbid alcohol and substance use disorders may play a role through toxicity effects in the outcomes of adult studies of hippocampal volumes and function (De Bellis et al., 2000
Poorer visual memory was significantly related to more PTSS, which may impair an individual’s ability to focus and maintain a representation of an object or event. This may lead to difficulty processing the traumatic event. Although studies in adult PTSD consistently report poorer visual and verbal memory function in PTSD (Brewin, Kleiner, Vasterling, & Field, 2007
; Gollier et al., 2005
; Koso & Hansen, 2006
) even when controlling for alcohol use disorder history (Samuelson et al., 2006
), specific memory indexes are understudied in pediatric PTSD. In one pilot study, children who suffered from maltreatment-related PTSD demonstrated significant deficits in attention and abstract reasoning/executive functions, which involve parietal and prefrontal cortices, when compared with non-maltreated healthy children (Beers & De Bellis, 2002
). Long-delay free recall on the California Verbal Learning Test was poorer in these children; however, this finding did not survive after corrections to protect from experiment-wise error. This is similar to our findings here of verbal memory not being predictive of total PTSD symptoms in the hierarchical modeling. In one study of children and adolescents with PTSD, lower verbal memory but no differences in other memory indexes were seen (Yasik, Saigh, Oberfield, & Halamandaris, 2007
). In another case–control study of South African adolescents, cognitive deficiencies were seen in attention, visual memory, and nonverbal concept formation that were associated with PTSD symptoms rather than trauma history (Schoeman, Carey, & Seedat, 2009
). Our finding of a negative relationship between visual memory and greater number of PTSD symptoms support the adult PTSD literature and most of the limited pediatric PTSD literature to date.
Trauma-focused cognitive behavioral therapy (CBT), the evidenced-based and most studied CBT treatment intervention in children with impairing PTSD symptoms, most likely strengthens an individual’s ability to focus through prefrontal inhibition of amygdala fear conditioned processes. Trauma-focused CBT is not enhanced by the use of psychotropics (Cohen, Mannarino, Perel, & Staron, 2007
). Our findings suggest that CBT interventions may further benefit from the use of evidence-based visual memory enhancement interventions, particularly in more symptomatic individuals.
Our finding that more CPT-II Errors of Commission was marginally associated with more PTSD symptoms is interesting in that impulsivity is frequently seen in clinical cases of PTSD, but inhibitory control or impulsivity is not a criteria symptom for PTSD. Perhaps inhibitory control should be evaluated as a criteria symptom for PTSD in children and adolescents. Interventions that are aimed at improving inhibitory control may enhance PTSD treatment.
Since our overall rate of PTSD in maltreated children and adolescents was relatively high, these data show that children are more vulnerable than adults to PTSD symptoms (De Bellis, 2001
). This finding is consistent with most of the available literature except for an epidemiological study which used the Child and Adolescent Psychiatric Assessment (Copeland et al., 2007
), an instrument that was not specifically designed for evaluating PTSD because it does not use a trauma narrative in its approach. In this epidemiological study, cumulative trauma predicted more depression and generalized anxiety symptoms, symptoms which overlap significantly with PTSD. It is important to identify PTSD in individuals with trauma histories and diagnoses of major depression and generalized anxiety disorder because trauma-focused CBT is an appropriate and specific evidenced-based treatment for these individuals, whereas the treatments for depression with comorbid generalized anxiety are relatively non-specific.
In our cross-sectional study of pediatric maltreatment, we cannot establish causal relationships between traumatic events, PTSD symptoms, and psychobiological differences. Our findings suggest the need for larger samples, longitudinal, and multi-site research by developmentally trained investigators that integrate expert clinical diagnostic evaluations with developmental and cognitive neuroscience. This type of work can include path analysis models, where the strength of these relationships and their interactions could be evaluated with respect to risk and resiliency factors for PTSD symptoms. Developmental traumatology model hypotheses can only be tested in a large sample longitudinal study that will clearly pave the way to better clinical treatment of pediatric PTSD in the future.