Browsing by Author "Gold, Andrea L"

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    Acute effects of trauma-focused research procedures on participant safety and distress
    (Psychiatry Research, 2014-01-30) Brown, Vanessa M; Strauss, Jennifer L; LaBar, Kevin S; Gold, Andrea L; McCarthy, Gregory; Morey, Rajendra A
    The ethical conduct of research on posttraumatic stress disorder (PTSD) requires assessing the risks to study participants. Some previous findings suggest that patients with PTSD report higher distress compared to non-PTSD participants after trauma-focused research. However, the impact of study participation on participant risk, such as suicidal/homicidal ideation and increased desire to use drugs or alcohol, has not been adequately investigated. Furthermore, systematic evaluation of distress using pre- and post-study assessments, and the effects of study procedures involving exposure to aversive stimuli, are lacking. Individuals with a history of PTSD (n=68) and trauma-exposed non-PTSD controls (n=68) responded to five questions about risk and distress before and after participating in research procedures including a PTSD diagnostic interview and a behavioral task with aversive stimuli consisting of mild electrical shock. The desire to use alcohol or drugs increased modestly with study participation among the subgroup (n=48) of participants with current PTSD. Participation in these research procedures was not associated with increased distress or participant risk, nor did study participation interact with lifetime PTSD diagnosis. These results suggest some increase in distress with active PTSD but a participant risk profile that supports a favorable risk-benefit ratio for conducting research in individuals with PTSD. © 2013.
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    Altered resting-state functional connectivity of basolateral and centromedial amygdala complexes in posttraumatic stress disorder.
    (Neuropsychopharmacology, 2014-01) Brown, Vanessa M; LaBar, Kevin S; Haswell, Courtney C; Gold, Andrea L; Mid-Atlantic MIRECC Workgroup; McCarthy, Gregory; Morey, Rajendra A
    The amygdala is a major structure that orchestrates defensive reactions to environmental threats and is implicated in hypervigilance and symptoms of heightened arousal in posttraumatic stress disorder (PTSD). The basolateral and centromedial amygdala (CMA) complexes are functionally heterogeneous, with distinct roles in learning and expressing fear behaviors. PTSD differences in amygdala-complex function and functional connectivity with cortical and subcortical structures remain unclear. Recent military veterans with PTSD (n=20) and matched trauma-exposed controls (n=22) underwent a resting-state fMRI scan to measure task-free synchronous blood-oxygen level dependent activity. Whole-brain voxel-wise functional connectivity of basolateral and CMA seeds was compared between groups. The PTSD group had stronger functional connectivity of the basolateral amygdala (BLA) complex with the pregenual anterior cingulate cortex (ACC), dorsomedial prefrontal cortex, and dorsal ACC than the trauma-exposed control group (p<0.05; corrected). The trauma-exposed control group had stronger functional connectivity of the BLA complex with the left inferior frontal gyrus than the PTSD group (p<0.05; corrected). The CMA complex lacked connectivity differences between groups. We found PTSD modulates BLA complex connectivity with prefrontal cortical targets implicated in cognitive control of emotional information, which are central to explanations of core PTSD symptoms. PTSD differences in resting-state connectivity of BLA complex could be biasing processes in target regions that support behaviors central to prevailing laboratory models of PTSD such as associative fear learning. Further research is needed to investigate how differences in functional connectivity of amygdala complexes affect target regions that govern behavior, cognition, and affect in PTSD.
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    Amygdala volume changes in posttraumatic stress disorder in a large case-controlled veterans group.
    (Arch Gen Psychiatry, 2012-11) Morey, Rajendra A; Gold, Andrea L; LaBar, Kevin S; Beall, Shannon K; Brown, Vanessa M; Haswell, Courtney C; Nasser, Jessica D; Wagner, H Ryan; McCarthy, Gregory; Mid-Atlantic MIRECC Workgroup
    CONTEXT: Smaller hippocampal volumes are well established in posttraumatic stress disorder (PTSD), but the relatively few studies of amygdala volume in PTSD have produced equivocal results. OBJECTIVE: To assess a large cohort of recent military veterans with PTSD and trauma-exposed control subjects, with sufficient power to perform a definitive assessment of the effect of PTSD on volumetric changes in the amygdala and hippocampus and of the contribution of illness duration, trauma load, and depressive symptoms. DESIGN: Case-controlled design with structural magnetic resonance imaging and clinical diagnostic assessments. We controlled statistically for the important potential confounds of alcohol use, depression, and medication use. SETTING: Durham Veterans Affairs Medical Center, which is located in proximity to major military bases. PATIENTS: Ambulatory patients (n = 200) recruited from a registry of military service members and veterans serving after September 11, 2001, including a group with current PTSD (n = 99) and a trauma-exposed comparison group without PTSD (n = 101). MAIN OUTCOME MEASURE: Amygdala and hippocampal volumes computed from automated segmentation of high-resolution structural 3-T magnetic resonance imaging. RESULTS: Smaller volume was demonstrated in the PTSD group compared with the non-PTSD group for the left amygdala (P = .002), right amygdala (P = .01), and left hippocampus (P = .02) but not for the right hippocampus (P = .25). Amygdala volumes were not associated with PTSD chronicity, trauma load, or severity of depressive symptoms. CONCLUSIONS: These results provide clear evidence of an association between a smaller amygdala volume and PTSD. The lack of correlation between trauma load or illness chronicity and amygdala volume suggests that a smaller amygdala represents a vulnerability to developing PTSD or the lack of a dose-response relationship with amygdala volume. Our results may trigger a renewed impetus for investigating structural differences in the amygdala, its genetic determinants, its environmental modulators, and the possibility that it reflects an intrinsic vulnerability to PTSD.
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    Serotonin transporter gene polymorphisms and brain function during emotional distraction from cognitive processing in posttraumatic stress disorder.
    (BMC Psychiatry, 2011-05-05) Morey, Rajendra A; Hariri, Ahmad R; Gold, Andrea L; Hauser, Michael A; Munger, Heidi J; Dolcos, Florin; McCarthy, Gregory
    BACKGROUND: Serotonergic system dysfunction has been implicated in posttraumatic stress disorder (PTSD). Genetic polymorphisms associated with serotonin signaling may predict differences in brain circuitry involved in emotion processing and deficits associated with PTSD. In healthy individuals, common functional polymorphisms in the serotonin transporter gene (SLC6A4) have been shown to modulate amygdala and prefrontal cortex (PFC) activity in response to salient emotional stimuli. Similar patterns of differential neural responses to emotional stimuli have been demonstrated in PTSD but genetic factors influencing these activations have yet to be examined. METHODS: We investigated whether SLC6A4 promoter polymorphisms (5-HTTLPR, rs25531) and several downstream single nucleotide polymorphisms (SNPs) modulated activity of brain regions involved in the cognitive control of emotion in post-9/11 veterans with PTSD. We used functional MRI to examine neural activity in a PTSD group (n = 22) and a trauma-exposed control group (n = 20) in response to trauma-related images presented as task-irrelevant distractors during the active maintenance period of a delayed-response working memory task. Regions of interest were derived by contrasting activation for the most distracting and least distracting conditions across participants. RESULTS: In patients with PTSD, when compared to trauma-exposed controls, rs16965628 (associated with serotonin transporter gene expression) modulated task-related ventrolateral PFC activation and 5-HTTLPR tended to modulate left amygdala activation. Subsequent to combat-related trauma, these SLC6A4 polymorphisms may bias serotonin signaling and the neural circuitry mediating cognitive control of emotion in patients with PTSD. CONCLUSIONS: The SLC6A4 SNP rs16965628 and 5-HTTLPR are associated with a bias in neural responses to traumatic reminders and cognitive control of emotions in patients with PTSD. Functional MRI may help identify intermediate phenotypes and dimensions of PTSD that clarify the functional link between genes and disease phenotype, and also highlight features of PTSD that show more proximal influence of susceptibility genes compared to current clinical categorizations.