Traumatic stress: effects on the brain
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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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 · 2.83 Impact Factor
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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 · 4.09 Impact Factor
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ABSTRACT: Pretreatment cognitive impairment in cancer patients is well established but unexplained. Similar cognitive compromise has been observed in post-traumatic stress disorder (PTSD) patients, and PTSD symptoms are a frequent concomitant of cancer diagnosis. We tested the hypothesis that pretreatment cognitive impairment is attributable to cancer-related post-traumatic stress. Women aged 65 years or younger who were diagnosed with breast cancer (case patients) or had undergone negative routine breast imaging (control patients) at one of six participating breast centers underwent traditional and computerized neuropsychological testing, clinician-administered diagnostic assessment of stress disorders, and self-report assessments of cognitive function and depression. To minimize confounding, case patients were evaluated prior to any local or systemic treatment. Cognitive indices of case patients, control patients, and normative samples were compared. The patients' risk of overall cognitive impairment was determined. Linear regression and a mediation model were used to test the study hypothesis. All statistical tests were two-sided. The 166 case patients and 60 well-matched control patients showed near-identical deviations from population norms. Case patients scored worse than control patients on two of 20 cognitive indices (Go/Nogo commission errors, Go/Nogo omission errors). Self-reported cognitive problems were associated with Go/Nogo omission errors and more pronounced in case patients. Only PTSD symptoms (Beta = 0.27, P = .004) and age (Beta = 0.22, P = .04) statistically significantly predicted Go/Nogo errors. The effect of having cancer on Go/Nogo errors was mediated by PTSD symptoms. Case patients did not have an increased risk of overall cognitive impairment. Prior to any treatment, breast cancer patients may show limited cognitive impairment that is apparently largely caused by cancer-related post-traumatic stress. © The Author 2015. Published by Oxford University Press. All rights reserved. For Permissions, please e-mail: firstname.lastname@example.org.CancerSpectrum Knowledge Environment 07/2015; 107(7). DOI:10.1093/jnci/djv099 · 15.16 Impact Factor