The impact of torture on interpersonal threat and reward neurocircuitry.

OBJECTIVE: Torture adversely influences emotional functioning, but the neurophysiological mechanisms underpinning its impact are unknown. This study examined how torture exposure affects the neural substrates of interpersonal threat and reward processing. METHODS: Male refugees with (N = 31) and without (N = 27) torture exposure completed a clinical interview and functional magnetic resonance imaging scan where they viewed fear, happy and neutral faces. Between-group activations and neural coupling were examined as moderated by posttraumatic stress disorder symptom severity and cumulative trauma load. RESULTS: Posttraumatic stress disorder symptom severity and trauma load significantly moderated group differences in brain activation and connectivity patterns. Torture survivors deactivated the ventral striatum during happy processing compared to non-torture survivor controls as a function of increased posttraumatic stress disorder symptom severity - particularly avoidance symptoms. The ventral striatum was more strongly coupled with the inferior frontal gyrus in torture survivors. Torture survivors also showed left hippocampal deactivation to both fear and happy faces, moderated by trauma load, compared to controls. Stronger coupling between the hippocampus and frontal, temporoparietal and subcortical regions during fear processing was observed, with pathways being predicted by avoidance and hyperarousal symptoms. CONCLUSION: Torture exposure was associated with distinct brain activity and connectivity patterns during threat and reward processing, dependent on trauma exposure and posttraumatic stress disorder symptom severity. Torture appears to affect emotional brain functioning, and findings have the potential to guide more targeted interventions for torture survivors.

Complex Posttraumatic Stress Disorder Symptom Profiles in Traumatized Refugees.

Although it is well documented that exposure to severe, cumulative trauma and postdisplacement stress increases the risk for posttraumatic stress symptom disorder (PTSD), less is known about the representation and predictors of complex PTSD (CPTSD) symptoms in refugee populations. We examined PTSD and CPTSD symptom profiles (co-occurring PTSD and disturbances in self-organization [DSO] symptoms) and their premigration, postmigration, and demographic predictors, using latent class analysis (LCA), in a cohort of 112 refugees resettled in Australia. The LCA identified a four-factor model as the best fit to the data, comprising classes categorized as: (a) CPTSD, exhibiting high levels of PTSD and DSO symptoms (29.5%); (b) PTSD only (23.5%); (c) high affective dysregulation (AD) symptoms (31.9%); and (d) low PTSD and DSO symptoms (15.1%). Membership in the CPTSD and PTSD classes was specifically associated with cumulative traumatization, CPTSD OR = 1.56, 95% CI [1.15, 2.12], and PTSD OR = 1.64, 95% CI [1.15, 2.34]; and female gender, CPTSD OR = 14.18, 95% CI [1.66, 121.29], and PTSD OR = 16.84, 95% CI [1.78, 159.2], relative to the low-symptom class. Moreover, CPTSD and AD class membership was significantly predicted by insecure visa status, CPTSD OR = 7.53, 95% CI [1.26, 45.08], and AD OR = 7.19, 95% CI [1.23, 42.05]. These findings are consistent with the ICD-11 model of CPTSD and highlight the contributions of cumulative trauma to CPTSD and PTSD profiles as well as of contextual stress from visa uncertainty to DSO symptom profiles in refugee cohorts, particularly those characterized by AD.

Spanish Abstracts by Asociación Chilena de Estrés Traumático (ACET) Perfiles de Síntomas de Trastorno de Estrés Postraumático Complejo en Refugiados Traumatizados PERFILES DE SÍNTOMAS DE TEPT COMPLEJO EN REFUGIADOS TRAUTATIZADOS Aunque está bien documentado que la exposición a trauma severo y acumulativo y el estrés posterior al desplazamiento en poblaciones de refugiados aumenta el riesgo de trastorno por síntomas de estrés postraumático (TEPT), se conoce menos acerca de la representación y los predictores de síntomas del TEPT complejo (TEPT-C). Examinamos los perfiles de síntomas de TEPT y TEPT-C (TEPT concurrente y síntomas de alteraciones en la auto-organización [DSO en su sigla en inglés]) y su pre-migración, post-migración y predictores demográficos, utilizando el análisis de clases latentes (ACL), en una cohorte de 112 refugiados reasentados en Australia. El ACL identificó un modelo de cuatro factores como el que mejor se ajusta a los datos, que comprende clases clasificadas tales como: (a) TEPT-C, que exhiben altos niveles de síntomas de TEPT y DSO (29.5%); (b)TEPT (23.5%); (c) síntomas de alta desregulación afectiva (DA) (31,9%); y (d) síntomas bajos de TEPT y DSO (15,1%). La adscripción en las clases de TEPT-C y TEPT se asociaron específicamente con traumatización acumulativa, TEPT-C OR = 1.56, IC 95% [1.15, 2.12] y TEPT OR = 1.64, IC 95% [1.15, 2.34]; y género femenino, TEPT-C OR = 14.18, IC 95% [1.66, 121.29], y TEPT OR = 16.84, IC 95% [1.78, 159.2], en relación con la clase de síntomas bajos. Además, la adscripción a la clase TEPT-C y AD se predijo significativamente por la inseguridad en el estado de su visa, TEPT-C OR = 7.53, IC 95% [1.26, 45.08], y AD OR = 7.19, IC 95% [1.23, 42.05]. Estos hallazgos son consistentes con el modelo CIE-11 de TEPT-C y destacan las contribuciones del trauma acumulativo a los perfiles de TEPT-C y TEPT, así como del estrés contextual desde la incertidumbre del estado de las visas hasta los perfiles de síntomas de DSO en cohortes de refugiados, particularmente en aquellos caracterizados por DA.

Teens that fear screams: A comparison of fear conditioning, extinction, and reinstatement in adolescents and adults.

This study investigated differences between adolescents and adults on fear conditioning, extinction, and reinstatement (i.e., the recovery of conditioned fear following re-exposure to the unconditioned stimulus [US] post-extinction). Participants underwent differential conditioning (i.e., the Screaming Lady) where one neutral face (CS+) was followed by the same face expressing fear and a loud scream (US) while another neutral face (CS-) remained neutral. Extinction involved non-reinforced presentations of both CSs, after which participants were reinstated (2xUSs) or not. On two self-report measures, both ages showed conditioning, good extinction learning and retention, and reinstatement-induced relapse. However, only adolescents showed conditioning, extinction, and reinstatement on the eye tracking measure; relapse on this measure could not be assessed in adults given they did not show initial conditioning. Lastly, higher levels of depression predicted stronger conditioning and weaker extinction in adolescents only. These findings are discussed in terms of their implications for adolescent anxiety disorders.

A window of vulnerability: impaired fear extinction in adolescence.

There have been significant advances made towards understanding the processes mediating extinction of learned fear. However, despite being of clear theoretical and clinical significance, very few studies have examined fear extinction in adolescence, which is often described as a developmental window of vulnerability to psychological disorders. This paper reviews the relatively small body of research examining fear extinction in adolescence. A prominent finding of this work is that adolescents, both humans and rodents, exhibit a marked impairment in extinction relative to both younger (e.g., juvenile) and older (e.g., adult) groups. We then review some potential mechanisms that could produce the striking extinction deficit observed in adolescence. For example, one neurobiological candidate mechanism for impaired extinction in adolescence involves changes in the functional connectivity within the fear extinction circuit, particularly between prefrontal cortical regions and the amygdala. In addition, we review research on emotion regulation and attention processes that suggests that developmental changes in attention bias to threatening cues may be a cognitive mechanism that mediates age-related differences in extinction learning. We also examine how a differential reaction to chronic stress in adolescence impacts upon extinction retention during adolescence as well as in later life. Finally, we consider the findings of several studies illustrating promising approaches that overcome the typically-observed extinction impairments in adolescent rodents and that could be translated to human adolescents.

Enhanced sensitivity to learning fearful associations during adolescence.

The majority of anxiety disorders emerge during adolescence, yet there is a paucity of research examining factors that contribute to the "storm and stress" of this period. Understanding how juvenile (P23), adolescent (P35), and adult (P90) rats differ on basic fear conditioning tasks may shed light on this issue. In Experiment 1, P23, P35, and P90 rats were given 6 CS-US presentations. There were four training conditions: Delay (i.e., CS co-terminating with the US), Trace 20 and Trace 40 (i.e., an interval of 20s and 40s between the CS and US, respectively), and Unpaired (i.e., explicitly Unpaired presentations of the CS and US). Twenty-four hours after conditioning, freezing was measured to assess fear of the CS in a novel context. At test, there were no age differences in CS-elicited freezing in group Delay, and this condition exhibited significantly higher levels of freezing compared to group Unpaired. However, the adolescent rats were the only age group to exhibit higher levels of freezing following training with the 20s and 40s trace intervals, compared to Unpaired controls. Experiment 2 replicated the finding that adolescent but not adult rats exhibit fear following conditioning with a 20s trace interval, while also demonstrating that both age groups display learning with a shorter trace interval of 5s. Experiment 3 showed that exposure to corticosterone (200 µg/ml) in the drinking water for 1 week prior to conditioning selectively disrupts Trace 20 but not Delay conditioning during adolescence. Lastly, in Experiment 4 the test procedures were changed such that freezing was measured both during the CS and during a stimulus free trace interval. Once again, P35 but not P90 rats exhibited fear following training with a 20s trace interval. Taken together, these findings demonstrate that adolescent rats show a heightened propensity to learn fearful associations, and that this is disrupted following exposure to corticosterone.

Opponent intrinsic brain network connectivity profiles associated with posttraumatic fear and dysphoria symptoms in trauma-exposed refugees.

OBJECTIVE: Resting-state functional magnetic resonance imaging (rsfMRI) studies report functional alterations in the connectivity between intrinsic brain networks in posttraumatic stress disorder (PTSD), but PTSD heterogeneity is rarely considered. Evidence points to fear (e.g., reexperiencing) and dysphoria (e.g., withdrawal) symptom factors as important in PTSD presentations, including relating to variable emotion dysregulation patterns. This study, therefore, tested how fear and dysphoria posttraumatic symptoms were differentially associated with core network connectivity and emotion dysregulation behaviors in a large group of trauma-exposed refugees. METHOD: A final sample of 77 trauma-exposed participants completed a rsfMRI scan. Independent component analysis identified active networks and functional network connectivity (FNC) between networks was assessed. Fear and dysphoria posttraumatic symptoms were partially correlated with FNCs, and linear regression models examined relationships with self-reported difficulties in emotion regulation. RESULTS: Twenty-three active networks were identified, eight being in the networks of interest (p < .05 false discovery rate-corrected). Fear and dysphoria symptoms were specifically related to connectivity patterns between two subnetworks of the default mode network (DMN). Fear symptoms were negatively associated with anterior dorsomedial DMN (admDMN) and temporoparietal DMN (tpDMN) connectivity; whereas dysphoria symptoms were positively associated with admDMN-tpDMN connectivity. Additionally, admDMN-tpDMN connectivity was positively predicted by goal-directed emotion dysregulation but negatively predicted by poor emotional clarity. CONCLUSIONS: Fear and dysphoria posttraumatic symptoms showed opponent associations with admDMN and tpDMN connectivity, potentially reflecting patterns of under- and overemotion dysregulation associated with these symptom profiles respectively. Findings highlight the importance of considering posttraumatic heterogeneity when constructing neural models of PTSD. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

Refugee visa insecurity disrupts the brain's default mode network.

BACKGROUND: Research has largely focused on the psychological consequences of refugee trauma exposure, but refugees living with visa insecurity face an uncertain future that also adversely affects psychological functioning and self-determination. OBJECTIVE: This study aimed to examine how refugee visa insecurity affects the functional brain. METHOD: We measured resting state brain activity via fMRI in 47 refugees with insecure visas (i.e. temporary visa status) and 52 refugees with secure visas (i.e. permanent visa status) residing in Australia, matched on key demographic, trauma exposure and psychopathology. Data analysis comprised independent components analysis to identify active networks and dynamic functional causal modelling tested visa security group differences in network connectivity. RESULTS: We found that visa insecurity specifically affected sub-systems within the default mode network (DMN) - an intrinsic network subserving self-referential processes and mental simulations about the future. The insecure visa group showed less spectral power in the low frequency band in the anterior ventromedial DMN, and reduced activity in the posterior frontal DMN, compared to the secure visa group. Using functional dynamic causal modelling, we observed positive coupling between the anterior and posterior midline DMN hubs in the secure visa group, while the insecure visa group displayed negative coupling that correlated with self-reported fear of future deportation. CONCLUSIONS: Living with visa-related uncertainty appears to undermine synchrony between anterior-posterior midline components of the DMN responsible for governing the construction of the self and making mental representations of the future. This could represent a neural signature of refugee visa insecurity, which is marked by a perception of living in limbo and a truncated sense of the future.

Refugee visa insecurity disrupts default mode network (DMN) connectivity ­ a core network that supports the internal construction of the self.Refugees living with insecure visa status showed decreased connectivity in the DMN and more negative coupling between midline anterior­posterior hubs of the DMN, compared to refugees living with secure visas.Diminished DMN connectivity may represent a neural basis for the psychological effects of refugee visa insecurity, which is associated with prolonged uncertainty regarding the future self and increased risk for psychological distress.

Torture exposure and the functional brain: investigating disruptions to intrinsic network connectivity using resting state fMRI.

Torture has profound psychological and physiological consequences for survivors. While some brain structures and functions appear altered in torture survivors, it is unclear how torture exposure influences functional connectivity within and between core intrinsic brain networks. In this study, 37 torture survivors (TS) and 62 non-torture survivors (NTS) participated in a resting-state fMRI scan. Data-driven independent components analysis identified active intrinsic networks. Group differences in functional connectivity in the default mode network (DMN), salience network (SN) and central executive network (CEN) of the triple network model, as well any prefrontal network, were examined while controlling for PTSD symptoms and exposure to other potentially traumatic events. The analysis identified 25 networks; eight comprised our networks of interest. Within-network group differences were observed in the left CEN (lCEN), where the TS group showed less spectral power in the low-frequency band. Differential internetwork dynamic connectivity patterns were observed, where the TS group showed stronger positive coupling between the lCEN and anterior dorsomedial and ventromedial DMN, and stronger negative coupling between a lateral frontal network and the lCEN and anterior dorsomedial DMN (when contrasted with the NTS group). Group differences were not attributed to torture severity or dissociative symptoms. Torture survivors showed disrupted dynamic functional connectivity between a laterally-aligned lCEN that serves top-down control functions over external processes and the midline DMN that underpins internal self-referential processes, which may be an adaptive response to mitigate the worst effects of the torture experience. This study provides a critical step in mapping the neural signature of torture exposure to guide treatment development and selection.

Activating the attachment system modulates neural responses to threat in refugees with PTSD.

Social attachment systems are disrupted for refugees through trauma and forced displacement. This study tested how the attachment system mitigates neural responses to threat in refugees with posttraumatic stress disorder (PTSD). Refugees with PTSD (N = 28) and refugee trauma-exposed controls (N = 22) viewed threat-related stimuli primed by attachment cues during a functional magnetic resonance imaging scan. Group differences and the moderating effects of avoidant or anxious attachment style and grief related to separation from family on brain activity and connectivity patterns were examined. Separation grief was associated with increased amygdala but decreased ventromedial prefrontal cortical (VMPFC) activity to the attachment prime and decreased VMPFC and hippocampal activity to attachment primed threat in the PTSD (vs trauma-exposed control) group. Avoidant attachment style was connected with increased dorsal frontoparietal attention regional activity to attachment prime cues in the PTSD group. Anxious attachment style was associated with reduced left amygdala connectivity with left medial prefrontal regions to attachment primed threat in the PTSD group. Separation grief appears to reduce attachment buffering of threat reactivity in refugees with PTSD, while avoidant and anxious attachment style modulated attentional and prefrontal regulatory mechanisms in PTSD, respectively. Considering social attachments in refugees could be important to post-trauma recovery, based within changes in key emotion regulation brain systems.

High endogenous estradiol is associated with enhanced cognitive emotion regulation of physiological conditioned fear responses in women.

The sex hormone estradiol has a modifying role in the underlying neurobiology of cognitive emotion regulation, although whether estradiol is associated with outcomes of techniques like cognitive restructuring is unknown. In the present study 34 women with regular menstrual cycles participated in a one-day differential fear conditioning procedure. Women then received cognitive restructuring training, involving the reappraisal of their initial thoughts about the conditioning procedure to reduce their emotional responses, before repeating the conditioning procedure. Endogenous estradiol levels (ascertained by a blood sample) were not associated with subjective or physiological indices of conditioned fear during the first conditioning session. Following cognitive restructuring, however, women with high estradiol exhibited significantly reduced physiological arousal in the presence of the conditioned stimulus, relative to women with low estradiol. No group differences were observed in subjective fear ratings obtained after the second conditioning procedure, although those obtained during the second habitation phase (taking place immediately following cognitive restructuring) were lower amongst high estradiol women. Progesterone was not associated with any outcomes measures. Together, these results suggest that the outcomes of cognitive emotion regulation may be enhanced during periods of naturally high estradiol.

A comparison of the short- and long-term effects of corticosterone exposure on extinction in adolescence versus adulthood.

Human and nonhuman adolescents have impaired retention of extinction of learned fear, relative to juveniles and adults. It is unknown whether exposure to stress affects extinction differently in adolescents versus adults. These experiments compared the short- and long-term effects of exposure to the stress-related hormone corticosterone (CORT) on the extinction of learned fear in adolescent and adult rats. Across all experiments, adolescent and adult rats were trained to exhibit good extinction retention by giving extinction training across 2 consecutive days. Despite this extra training, adolescents exposed to 1 week of CORT (200 µg/ml) in their drinking water showed impaired extinction retention when trained shortly after the CORT was removed (Experiment 1a). In contrast, adult rats exposed to CORT (200 µg/ml) for the same duration did not exhibit deficits in extinction retention (Experiment 1b). Exposing adolescents to half the amount of CORT (100 µg/ml; Experiment 1c) for 1 week similarly disrupted extinction retention. Extinction impairments in adult rats were only observed after 3 weeks, rather than 1 week, of CORT (200 µg/ml; Experiment 1d). Remarkably, however, adult rats showed impaired extinction retention if they had been exposed to 1 week of CORT (200 µg/ml) during adolescence (Experiment 2). Finally, exposure to 3 weeks of CORT (200 µg/ml) in adulthood led to long-lasting extinction deficits after a 6-week drug-free period (Experiment 3). These findings suggest that although CORT disrupts both short- and long-term extinction retention in adolescents and adults, adolescents may be more vulnerable to these effects because of the maturation of stress-sensitive brain regions. (PsycINFO Database Record (c) 2014 APA, all rights reserved).