Posttraumatic stress symptom persistence across 24 years: association with brain structures

Franz, Carol E.; Hatton, Sean N.; Hauger, Richard L.; Kredlow, M. Alexandra; Dale, Anders M.; Eyler, Lisa T.; McEvoy, Linda K.; Fennema-Notestine, Christine; Hagler, Donald J.; Jacobson, Kristen C.; McKenzie, Ruth; Panizzon, Matthew S.; Gustavson, Daniel E.; Xian, Hong; Toomey, Rosemary; Beck, Audrey N.; Stevens, Samantha; Tu, Xin; Lyons, Michael J.; Kremen, William S.

doi:10.1007/s11682-019-00059-x

Cited by 8 publications

(9 citation statements)

References 91 publications

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“…Specifically, we found associations between posttraumatic stress and accelerated thinning in the posterior cingulate, e.g., 48,49 depressive symptoms and faster thinning in the anterior cingulate, e.g., 50,51 and anxiety symptoms with slower surface area expansion in orbitofrontal and posterior cingulate. e.g., 52,53 In contrast to prior work, 16,54 posttraumatic stress was associated with increased expansion of hippocampal volumes in our study. Smaller hippocampal volumes are a known risk factor for developing persistent posttraumatic stress disorder among adults; 55 thus, it is possible that the increase in volume over time observed here is neuroprotective and supports resilience in these typically-developing youth.…”

Section: Discussioncontrasting

confidence: 99%

“…Past studies have primarily focused on gray matter volume, surface area, or cortical thickness in regions involved in social-emotional processes, and compared individuals with or without clinical diagnoses. 14,[16][17][18][19] More recent studies have examined the effects of anxiety and depressive symptom severity to better understand full spectra of symptom sets and their unique impacts on brain structure and function. 9,[20][21][22][23][24] Studies have generally shown that increasing anxiety or depressive symptom severity is associated with changes in gray matter, though the specific regions implicated are disparate across studies.…”

Section: Introductionmentioning

confidence: 99%

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Subclinical Anxiety and Posttraumatic Stress Influence Cortical Thinning During Adolescence

Taylor

Eastman

Frenzel

et al. 2021

Journal of the American Academy of Child & Adolescent Psych

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Section: Discussioncontrasting

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Subclinical Anxiety and Posttraumatic Stress Influence Cortical Thinning During Adolescence

Taylor

Eastman

Frenzel

et al. 2021

Journal of the American Academy of Child & Adolescent Psych

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“…The findings are in line with a recent study showing that amygdala reactivity immediately following the index trauma is related to PTSD symptoms months post-trauma 6 . In addition, previous studies have reported that amygdala reactivity to affective stimuli pre-deployment positively predicted post-deployment PTSD symptoms in military samples 52,53 , and that post-traumatic stress symptoms in the aftermath of an index trauma were negatively associated with total amygdala volume 24 years later 54 . The present study extends these findings by showing that the longterm lateral nucleus volume is associated with early symptom development, and indeed may mediate the association between short-and long-term outcome.…”

Section: Discussionmentioning

confidence: 95%

The association of PTSD symptom severity with amygdala nuclei volumes in traumatized youths

et al. 2020

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The amygdala is a core component in neurobiological models of stress and stress-related pathologies, including posttraumatic stress disorder (PTSD). While numerous studies have reported increased amygdala activity following traumatic stress exposure and in PTSD, the findings regarding amygdala volume have been mixed. One reason for these mixed findings may be that the amygdala has been considered as a homogenous entity, while it in fact consists of several nuclei with unique cellular and connectivity profiles. Here, we investigated amygdala nuclei volumes of the basolateral and the centrocorticomedial complex in relation to PTSD symptom severity in 47 young survivors from the 2011 Norwegian terror attack 24-36 months post-trauma. PTSD symptoms were assessed 4-5, 14-15 and 24-36 months following the trauma. We found that increased PTSD symptom severity 24-36 months post-trauma was associated with volumetric reductions of all basolateral as well as the central and the medial nuclei. However, only the lateral nucleus was associated with longitudinal symptom development, and mediated the association between 4-5 months and 24-36 months post-trauma symptoms. The results suggest that the amygdala nuclei may be differentially associated with cross-sectional and longitudinal measures of PTSD symptom severity. As such, investigations of amygdala total volume may not provide an adequate index of the association between amygdala and stress-related mental illness.

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“…In summary, developing PTSD symptoms in response to trauma put individuals at greater risk for worse quality of life outcomes decades later, which may ultimately contribute to increased risk for disease and mortality as they age [3,4,69]. We found, for instance, that PTSD symptoms from age 38 were associated with structural deficits in brain regions regulating stress responsivity and adaptation at midlife [70,71].…”

Section: Discussionmentioning

confidence: 74%

“…Stress mediators such as corticotropin releasing factor are implicated in anxiety and stress disorders and are moderately heritable [84][85][86][87]. Additionally, there is evidence that stress responses are associated with brain regions that play important roles in how events are perceived, experienced, interpreted, and managed [70,88,89]. Moreover, emerging evidence suggests genetic variation may increase risk for anxiety disorders and affect brain neurocircuitry [90].…”

Section: Discussionmentioning

confidence: 99%

Predicting Health-Related Quality of Life in Trauma-Exposed Male Veterans in Late Midlife: A 20 Year Longitudinal Study

Stevens

Gustavson

Fang

et al. 2020

IJERPH

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Trauma-exposed adults with high levels of posttraumatic stress symptoms (PTSS) report poorer health-related quality of life (HRQOL), but less is known about the persistence of this relationship over time. Participants from the Vietnam Era Twin Study of Aging reported on PTSS, health, and sociodemographic characteristics at average age 38; 775 participants reported having been exposed to trauma. Later, at average ages 56 and 62, mental and physical HRQOL were assessed with the Short-Form 36. Premorbid risk for anxiety/neuroticism was evaluated with a polygenic risk score derived from a large genome-wide association study meta-analysis. In multivariate mixed models, having higher levels of PTSS, poorer self-rated health, lower income, and less education at age 38 were associated with worse physical and mental HRQOL two decades later. Chronic health problems at age 38 predicted midlife physical but not mental HRQOL. Although genetic risk for neuroticism was correlated with HRQOL and PTSS, it was no longer significant in multivariate models. Health-related quality of life (HRQOL) predicts morbidity and mortality independently of objective health measures; early interventions may help to mitigate the ongoing impact of trauma on quality of life.

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Posttraumatic stress symptom persistence across 24 years: association with brain structures

Cited by 8 publications

References 91 publications

Subclinical Anxiety and Posttraumatic Stress Influence Cortical Thinning During Adolescence

Subclinical Anxiety and Posttraumatic Stress Influence Cortical Thinning During Adolescence

The association of PTSD symptom severity with amygdala nuclei volumes in traumatized youths

Predicting Health-Related Quality of Life in Trauma-Exposed Male Veterans in Late Midlife: A 20 Year Longitudinal Study

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