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

ABSTRACT 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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    • "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.
    Journal of Psychiatric Research 12/2014; 62. DOI:10.1016/j.jpsychires.2014.12.002
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    • "Increased levels of cortisol may affect both brain structure and function, leading to increased vulnerability to stress-related psychiatric disorders ( Phillips et al., 2006; Frodl and O'Keane, 2013). Indeed, higher cortisol levels in both humans and animals have been associated with hippocampal volume reductions over time, although not consistently (Hibberd et al., 2000; Coe et al., 2003; Brown et al., 2004; Frodl and O'Keane, 2013), and there are possible relations with post-traumatic stress disorder (Bremner, 2006) and early life maltreatment , both being associated with changes in the volume of the hippocampus and prefrontal cortex (Frodl and O'Keane, 2013). Increased cortisol levels and evidence of reduced negative feedback of the HPA axis, as indexed by the combined dexamethasone Contents lists available at ScienceDirect journal homepage: "
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    ABSTRACT: Stress and abnormal hypothalamic-pituitary-adrenal axis functioning have been implicated in the early phase of psychosis and may partly explain reported changes in brain structure. This study used magnetic resonance imaging to investigate whether biological measures of stress were related to brain structure at baseline and to structural changes over the first 12 weeks of treatment in first episode patients (n=22) compared with matched healthy controls (n=22). At baseline, no significant group differences in biological measures of stress, cortical thickness or hippocampal volume were observed, but a significantly stronger relationship between baseline levels of cortisol and smaller white matter volumes of the cuneus and anterior cingulate was found in patients compared with controls. Over the first 12 weeks of treatment, patients showed a significant reduction in thickness of the posterior cingulate compared with controls. Patients also showed a significant positive relationship between baseline cortisol and increases in hippocampal volume over time, suggestive of brain swelling in association with psychotic exacerbation, while no such relationship was observed in controls. The current findings provide some support for the involvement of stress mechanisms in the pathophysiology of early psychosis, but the changes are subtle and warrant further investigation. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.
    Psychiatry Research : Neuroimaging 11/2014; 231(2). DOI:10.1016/j.pscychresns.2014.11.004
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    • "Stress Diagnostic Scale (Foa et al. 1997). Participants who had been exposed to at least one traumatic experience in their lifespan, were excluded (N = 18), because prior trauma might influence amygdala and hippocampal structure (Bremner 2006). Trait anxiety was assessed using the State-Trait Anxiety Inventory, G-form X2 (Laux et al. 1981). "
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    ABSTRACT: Fear conditioning is a basic learning process which involves the association of a formerly neutral conditioned stimulus (CS) with a biologically relevant aversive unconditioned stimulus (US). Previous studies conducted in brain-lesioned patients have shown that while the acquisition of autonomic fear responses requires an intact amygdala, a spared hippocampus is necessary for the development of the CS-US contingency awareness. Although these data have been supported by studies using functional neuroimaging techniques in healthy people, attempts to extend these findings to the morphological aspects of amygdala and hippocampus are missing. Here we tested the hypothesis that amygdalar and hippocampal volumes play dissociable roles in determining autonomic responses and contingency awareness during fear conditioning. Fifty-two healthy individuals (mean age 21.83) underwent high-resolution magnetic resonance imaging. We used a differential delay fear conditioning paradigm while assessing skin conductance responses (SCRs), subjective ratings of CS-US contingency, as well as emotional valence and perceived arousal. Left amygdalar volume significantly predicted the magnitude of differential SCRs during fear acquisition, but had no impact on contingency learning. Conversely, bilateral hippocampal volumes were significantly related to contingency ratings, but not to SCRs. Moreover, left amygdalar volume predicted SCRs to the reinforced CS alone, but not those elicited by the US. Our findings bridge the gap between previous lesion and functional imaging studies, by showing that amygdalar and hippocampal volumes differentially modulate the acquisition of conditioned fear. Further, our results reveal that the morphology of these limbic structures moderate learning and memory already in healthy persons.
    Brain Structure and Function 06/2014; DOI:10.1007/s00429-014-0807-8
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