Traumatic stress: Effects on the brain

Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Ga 30306, USA.
Dialogues in clinical neuroscience 02/2006; 8(4):445-61.
Source: PubMed


Brain areas implicated in the stress response include the amygdala, hippocampus, and prefrontal cortex. Traumatic stress can be associated with lasting changes in these brain areas. Traumatic stress is associated with increased cortisol and norepinephrine responses to subsequent stressors. Antidepressants have effects on the hippocampus that counteract the effects of stress. Findings from animal studies have been extended to patients with post-traumatic stress disorder (PTSD) showing smaller hippocampal and anterior cingulate volumes, increased amygdala function, and decreased medial prefrontal/anterior cingulate function. In addition, patients with PTSD show increased cortisol and norepinephrine responses to stress. Treatments that are efficacious for PTSD show a promotion of neurogenesis in animal studies, as well as promotion of memory and increased hippocampal volume in PTSD.

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Available from: James Douglas Bremner, Jan 14, 2016
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    • "As PTSD duration has been proposed to impact brain structure and function [Bremner, 2006], exploratory analyses examined the association between PTSD duration and amygdalar connectivity and structure. Specifically, partial correlation analyses in PTSD patients (adjusted for age, sex, and IQ) examined the association between PTSD duration and subregional connectivity and volumetrics within areas of significant group differences. "
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    ABSTRACT: Posttraumatic stress disorder (PTSD) is a prevalent, debilitating, and difficult to treat psychiatric disorder. Very little is known of how PTSD affects neuroplasticity in the developing adolescent brain. Whereas multiple lines of research implicate amygdala-centered network dysfunction in the pathophysiology of adult PTSD, no study has yet examined the functional architecture of amygdala subregional networks in adolescent PTSD. Using intrinsic functional connectivity analysis, we investigated functional connectivity of the basolateral (BLA) and centromedial (CMA) amygdala in 19 sexually abused adolescents with PTSD relative to 23 matched controls. Additionally, we examined whether altered amygdala subregional connectivity coincides with abnormal grey matter volume of the amygdaloid complex. Our analysis revealed abnormal amygdalar connectivity and morphology in adolescent PTSD patients. More specifically, PTSD patients showed diminished right BLA connectivity with a cluster including dorsal and ventral portions of the anterior cingulate and medial prefrontal cortices (p < 0.05, corrected). In contrast, PTSD patients showed increased left CMA connectivity with a cluster including the orbitofrontal and subcallosal cortices (p < 0.05, corrected). Critically, these connectivity changes coincided with diminished grey matter volume within BLA and CMA subnuclei (p < 0.05, corrected), with CMA connectivity shifts additionally relating to more severe symptoms of PTSD. These findings provide unique insights into how perturbations in major amygdalar circuits could hamper fear regulation and drive excessive acquisition and expression of fear in PTSD. As such, they represent an important step toward characterizing the neurocircuitry of adolescent PTSD, thereby informing the development of reliable biomarkers and potential therapeutic targets. Hum Brain Mapp, 2016.
    Full-text · Article · Jan 2016 · Human Brain Mapping
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    • "However, the pathophysiological mechanisms underlying the development of neurobiological consequences of childhood trauma and its relationship to development of psychiatric illness have not been fully elucidated. Disruption of the hypothalamic-pituitaryadrenal (HPA) axis with subsequent cortisol induced toxicity has been proposed as one mechanism for some of the observed neuroimaging differences in this population (Bremner, 2006, 1999; Marin et al., 2007; McCrory et al., 2010). Another proposed mechanism is a trauma-induced inflammatory response which could lead to neuronal injury (Herberth et al., 2008; Miller et al., 2009). "
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    ABSTRACT: Serum levels of the astrocytic protein S100B have been reported to indicate disruption of the blood-brain barrier. In this study, we investigated the relationship between S100B levels and childhood trauma in a child psychiatric inpatient unit. Levels of S100B were measured in a group of youth with mood disorders or psychosis with and without history of childhood trauma as well as in healthy controls. Study participants were 93 inpatient adolescents admitted with a diagnosis of psychosis (N = 67), or mood disorder (N = 26) and 22 healthy adolescents with no history of trauma or psychiatric illness. Childhood trauma was documented using the Life Events Checklist (LEC) and Adverse Child Experiences (ACE). In a multivariate regression model, suicidality scores and trauma were the only two variables which were independently related to serum S100B levels. Patients with greater levels of childhood trauma had significantly higher S100B levels even after controlling for intensity of suicidal ideation. Patients with psychotic diagnoses and mood disorders did not significantly differ in their levels of S100B. Patients exposed to childhood trauma were significantly more likely to have elevated levels of S100B (p < .001) than patients without trauma, and patients with trauma had significantly higher S100B levels (p < .001) when compared to the control group. LEC (p = 0.046), and BPRS-C suicidality scores (p = 0.001) significantly predicted S100B levels. Childhood trauma can potentially affect the integrity of the blood-brain barrier as indicated by associated increased S100B levels. Copyright © 2014 Elsevier Ltd. All rights reserved.
    Full-text · Article · Dec 2014 · Journal of Psychiatric Research
    • "Studies in psychiatric patients report associations between HPA axis dysregulation and reduced HV (O'Brien et al., 2004; Swaab et al., 2005; Bremner, 2006; Karl et al., 2006). Among healthy populations, studies have revealed that smaller HV is associated with higher basal cortisol levels in young (Wolf et al., 2002; Vythilingam et al., 2004) and older adults (Lupien et al., 1998; Wolf et al., 2002; O'Hara et al., 2007; Bruehl et al., 2009; Knoops et al., 2010). "
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    ABSTRACT: The hypothalamic pituitary adrenal axis production of the stress hormone cortisol interacts with the hippocampal formation and impacts memory function. A growing interest is to determine whether hippocampal volume (HV) predicts basal and/or reactive cortisol levels in young and older adults. Recent evidence shows that contextual features in testing environments might be stressful and inadvertently induce a stress response in young and/or older populations. This latter result suggests that variations in testing environments might influence associations between HV and cortisol levels in young and older adults. To this end, we investigated 28 healthy young adults (ages 18 to 35) and 32 healthy older adults (ages 60 to 75) in two different environments constructed to be more or less stressful for each age group (Favouring-Young versus Favouring-Old conditions). Cortisol levels were repeatedly assessed in each environment, and young and older participants underwent an anatomical magnetic resonance imaging scan for subsequent assessment of HV. Results in both age groups showed that HV was significantly associated with cortisol levels only in the unfavourable stressful testing conditions specific for each age group. This association was absent when testing environments were designed to decrease stress for each age group. These findings are fundamental in showing that unless the nature of the testing environment is taken into consideration, detected associations between HV and cortisol levels in both young and older populations might be confounded by environmental stress. © 2014 Wiley Periodicals, Inc.
    No preview · Article · Dec 2014 · Hippocampus
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