Academic journal article European Journal of Psychotraumatology

Right Temporal Cortical Hypertrophy in Resilience to Trauma: An MRI Study

Academic journal article European Journal of Psychotraumatology

Right Temporal Cortical Hypertrophy in Resilience to Trauma: An MRI Study

Article excerpt

Posttraumatic stress disorder (PTSD) is caused by major life stressors such as accidents, war, or perceived threat to life. However, most people do not develop PTSD after a potential traumatic event (Kessler, 1995). Several factors predict susceptibility to PTSD such as age, gender, socio-economic status (Perkonigg, Kessler, Storz, & Wittchen, 2000), other life stressors, and comorbid mental disorders such as depression (Brewin, Andrews, & Valentine, 2000). Prevalence rates also vary between different kinds of event types, occupational roles of survivors, and even geographic locations (Berger et al., 2012; Darves-Bornoz et al., 2008; Norris, 1992). Most of these factors fall along the risk-resilience spectrum, as they are unlikely to change due to trauma exposure; however, when investigating physiological measures such as brain morphology, it is more difficult to distinguish what constitute risk-resilience factors and what the effects of trauma exposure and PTSD are.

Morphological studies of individuals with PTSD have implicated several regions, mostly along the fear circuitry model, including amygdala, hippocampus, prefrontal cortex (PFC), and anterior cingulate cortex (ACC) (Kuhn & Gallinat, 2013; Rauch, Shin, & Phelps, 2006; Shin & Handwerger, 2009). Several PTSD studies have also focused on the association between degree of trauma and morphology. One recent magnetic resonance imaging (MRI) study investigated people at various distances from 9/11 and observed an association between symptom load and gray matter volume in the amygdala, hippocampus, insula, PFC, and ACC, dependent on how far away subjects were from the twin towers (Ganzel, Kim, Glover, & Temple, 2008). A study of survivors in a coal mine accident found a negative association between the clinician-administered PTSD scale (CAPS) scores in PTSD-positive subjects and gray matter volume in the ACC (Chen et al., 2012). Gray matter volume of the frontal and temporal lobes has been implicated in combat veterans with PTSD (Geuze, Westenberg, et al., 2008), and the researchers observed a dissociation between cortical thickness and memory performance in PTSDpositive participants, but an association for PTSD-negative participants. In addition to these studies, a meta-analysis including nine studies of diverse forms of trauma found that PTSD-positive vs. PTSD-negative participants had lower gray matter volume in ACC, venteromedial PFC, left temporal pole/middle temporal gyrus, and left hippocampus (Kühn & Gallinat, 2013). On the contrary, Landre et al. (2010) observed no differences between non-combat PTSD-positive and healthy controls which cautions against assuming that results from one kind of trauma automatically generalizes to the next. In summary, most studies observe morphological differences in the hippocampus, amygdala, ACC, and PFC. However, similar regions have also been observed in studies of trauma survivors without PTSD.

Comparisons between trauma-exposed (TE) individuals without PTSD and healthy controls have revealed several regions of interest; a meta-analysis by Karl et al. (2006) implicated the amygdala, hippocampus, ACC, corpus callosum, and the frontal lobe, whereas another meta-analysis by Smith (2005) implicated hippocampus, while a recent review by O'Doherty et al. (2015) implicated the hippocampus and ACC, but not the amygdala. In summary, the amygdala, hippocampus, ACC, and prefrontal regions are heavily implicated in both the PTSD-positive and the PTSD-negative literature. Assuming that trauma exposure alone is not enough to cause observable longitudinal group differences in morphology, as indicated by a seminal prospective study by Van Wingen, Geuze, Vermetten, and Fernandez (2011), one hypothesis is that several of the above-implicated areas might be associated with risk-resilience factors rather than effects of trauma.

For instance, the PFC has been implicated as a resilience factor to stress and anxiety in rodents (Russo, Murrough, Han, Charney, & Nestler, 2012), and in another study on soldiers resilient to combat-related PTSD, researchers observed decreased activity in PFC and nucleus accumbens, and abnormal plasticity levels in hippocampus, amygdala, and PFC (Wu et al. …

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