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Brain and behavioral evidence for altered social learning mechanisms among women with assault-related posttraumatic stress disorder.

ABSTRACT: Current neurocircuitry models of PTSD focus on the neural mechanisms that mediate hypervigilance for threat and fear inhibition/extinction learning. Less focus has been directed towards explaining social deficits and heightened risk of revictimization observed among individuals with PTSD related to physical or sexual assault. The purpose of the present study was to foster more comprehensive theoretical models of PTSD by testing the hypothesis that assault-related PTSD is associated with behavioral impairments in a social trust and reciprocity task and corresponding alterations in the neural encoding of social learning mechanisms. Adult women with assault-related PTSD (n = 25) and control women (n = 15) completed a multi-trial trust game outside of the MRI scanner. A subset of these participants (15 with PTSD and 14 controls) also completed a social and non-social reinforcement learning task during 3T fMRI. Brain regions that encoded the computationally modeled parameters of value expectation, prediction error, and volatility (i.e., uncertainty) were defined and compared between groups. The PTSD group demonstrated slower learning rates during the trust game and social prediction errors had a lesser impact on subsequent investment decisions. PTSD was also associated with greater encoding of negative expected social outcomes in perigenual anterior cingulate cortex and bilateral middle frontal gyri, and greater encoding of social prediction errors in the left temporoparietal junction. These data suggest mechanisms of PTSD-related deficits in social functioning and heightened risk for re-victimization in assault victims; however, comorbidity in the PTSD group and the lack of a trauma-exposed control group temper conclusions about PTSD specifically.

SUBMITTER: Cisler JM

PROVIDER: S-EPMC4422332 | biostudies-literature | 2015 Apr

REPOSITORIES: biostudies-literature

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Brain and behavioral evidence for altered social learning mechanisms among women with assault-related posttraumatic stress disorder.

Cisler Josh M JM Bush Keith K Scott Steele J J Lenow Jennifer K JK Smitherman Sonet S Kilts Clinton D CD

Journal of psychiatric research 20150224

Current neurocircuitry models of PTSD focus on the neural mechanisms that mediate hypervigilance for threat and fear inhibition/extinction learning. Less focus has been directed towards explaining social deficits and heightened risk of revictimization observed among individuals with PTSD related to physical or sexual assault. The purpose of the present study was to foster more comprehensive theoretical models of PTSD by testing the hypothesis that assault-related PTSD is associated with behavior ...[more]

PMID: 25769397

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Project description:BackgroundFear responding in posttraumatic stress disorder (PTSD) is sexually heterogeneous and varies with hormonal fluctuations throughout the menstrual cycle. While research suggests that estrogen levels affect PTSD symptoms among women, there is a dearth of research on modulatory effects of estrogen on fear responding among women with PTSD, and neural outcome measures are lacking.MethodsA sample of 42 women with PTSD underwent 2 consecutive alternating blocks of fear conditioning and extinction training, during which a CS+ conditioned stimulus, but not a CS-, predicted the occurrence of an electric shock in an acquisition context but not in an extinction context. Assayed saliva determined estradiol levels. Skin conductance response and whole-brain voxelwise activity during functional magnetic resonance imaging were outcome variables in linear mixed-effects models, with estradiol level, PTSD severity, and task contrasts as predictors.ResultsSkin conductance response exhibited a significant estradiol × PTSD severity × habituation interaction (t = 3.180, p = .002), such that PTSD severity was correlated with increased arousal responding between training blocks among women with lower estradiol (t = -3.985, p < .001) but not higher estradiol (t = 0.550, p = .583). Voxelwise activity also demonstrated an identical three-way interaction within dorsomedial prefrontal cortex and anterior insula clusters. The skin conductance response and imaging interactions between PTSD severity and estradiol were not specific to conditioned stimulus type or context.ConclusionsEstradiol moderated the relationship between PTSD severity and arousal response habituation between fear conditioning and extinction training sessions, such that high estradiol protected against the negative impact of severe PTSD symptoms on fear habituation. These findings suggest that estrogen enhances habituation among women with severe PTSD, potentially influencing the efficacy of extinction-based therapies.

Project description:ImportanceLittle is known about the prevalence of traumatic exposures among midlife and older women and the association of these traumatic exposures with health issues.ObjectiveTo examine the associations of intimate partner violence (IPV), sexual assault, and posttraumatic stress with menopause symptoms among midlife and older women.Design, setting, and participantsA cross-sectional analysis of data from a multiethnic cohort of 2016 women 40 to 80 years of age in the Kaiser Permanente Northern California health care system was conducted from November 15, 2008, to March 30, 2012. Statistical analysis was conducted from June 8, 2016, to September 6, 2017.ExposuresLifetime physical or emotional IPV, sexual assault, and current symptoms of posttraumatic stress disorder, assessed with standardized questionnaires.Main outcomes and measuresDifficulty sleeping, vasomotor symptoms, and vaginal symptoms, assessed with standardized questionnaires.ResultsAmong the 2016 women enrolled, the mean (SD) age was 60.5 (9.5) years, and 792 of 2011 with race/ethnicity data (39.4)% were non-Latina white (403 [20.0%] Latina, 429 [21.3%] black, and 387 [19.2%] Asian). Lifetime emotional IPV was reported by 423 women (21.0%), lifetime physical IPV was reported by 316 women (15.7%), sexual assault was reported by 382 women (18.9%), and 450 of 2000 women (22.5%) had current clinically significant symptoms of posttraumatic stress disorder. In multivariable analyses adjusted for age, race/ethnicity, educational level, body mass index, menopause status, hormone therapy, and parity, symptoms of posttraumatic stress disorder were associated with difficulty sleeping (odds ratio [OR], 3.02; 95% CI, 2.22-4.09), vasomotor symptoms (hot flashes: OR, 1.69; 95% CI, 1.34-2.12; night sweats: OR, 1.72; 95% CI, 1.37-2.15), and vaginal symptoms (vaginal dryness: OR, 1.73; 95% CI, 1.37-2.18; vaginal irritation: OR, 2.20; 95% CI, 1.66-2.93; pain with intercourse: OR, 2.16; 95% CI, 1.57-2.98). Emotional IPV was associated with difficulty sleeping (OR, 1.36; 95% CI, 1.09-1.71), night sweats (OR, 1.50; 95% CI, 1.19-1.89), and pain with intercourse (OR, 1.60; 95% CI, 1.14-2.25). Physical IPV was associated with night sweats (OR, 1.33; 95% CI, 1.03-1.72). Sexual assault was associated with vaginal symptoms (vaginal dryness: OR, 1.41; 95% CI, 1.10-1.82; vaginal irritation: OR, 1.42; 95% CI, 1.04-1.95; pain with intercourse: OR, 1.44; 95% CI, 1.00-2.06).Conclusions and relevanceLifetime history of IPV or sexual assault and current clinically significant symptoms of posttraumatic stress disorder are common and are associated with menopause symptoms. These findings highlight the need for greater recognition of these exposures by clinicians caring for midlife and older women.

Project description:BACKGROUND:Posttraumatic stress disorder (PTSD) is associated with disturbed sleep and elevated levels of pro-inflammatory cytokines, including interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α). Studies in animals and healthy humans have also shown that disrupted sleep elevates pro-inflammatory cytokines, including IL-6 and TNF-α. A better understanding of overnight cytokine levels and sleep might shed light on possible mechanisms for elevated inflammation in PTSD. Thus, we investigated overnight levels of IL-6 and TNF-α in individuals with and without PTSD while recording sleep polysomnography (PSG). METHOD:Serum samples were collected from otherwise healthy, medication-free participants with chronic PTSD (n = 44; 50% female; M age = 30.34 ± 8.11) and matched controls (n = 49; 53% female; M age = 30.53 ± 6.57) during laboratory PSG. Levels of IL-6 and TNF-α were measured at hours 0, 2, 4, 6, and 8 after typical sleep onset time using serial serum samples. Plasma IL-6 and TNF-α levels were quantified using enzyme-linked immunosorbent assays. RESULTS:Growth model analysis indicated a significantgroup by time interaction for IL-6 (t[247] = -2.92, p = .005) and a significant group by sex by time interaction for TNF-α (t[275] = 2.02, p = .04). PTSD positive men and women initially had higher IL-6 and TNF-α at sleep onset, but not at the end of their sleep cycle. Men with PTSD showed a peak of TNF-α at the end of the sleep cycle, whereas male control subjects demonstrated an inverted U-shaped profile. There were no significant differences in TNF-α levels overnight between women with and without PTSD. CONCLUSION:To our knowledge, this is the largest study to examine IL-6 overnight in a PTSD sample and the first study to examine overnight TNF-α in PTSD. Overnight IL-6 and TNF-α levels may be altered in individuals with PTSD compared to those without PTSD, and TNF-α trajectories also differed by sex. The current findings highlight the need to consider sex, sleep, time of day, and circadian variation when examining inflammation in PTSD. Additional research in broader study samples will be necessary to clarify associations between disrupted sleep, cytokines, and increased risk for disease in PTSD.

Dataset Information

Brain and behavioral evidence for altered social learning mechanisms among women with assault-related posttraumatic stress disorder.

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Brain and behavioral evidence for altered social learning mechanisms among women with assault-related posttraumatic stress disorder.

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