Processing In Posttraumatic Stress Disorder Research Articles

Synergic Trio of Metabolic Regulators Supporting the Vicious Circle of Pathological Processes in Post-Traumatic Stress Disorder

Post-traumatic stress disorder (PTSD) is a maladaptive response to exposure of extreme intensity stressor. The body of animals and humans reacts at the systemic and cellular levels, as with any response to external challenges. Disorder of the collective work of stress-realizing and stress-limiting systems causes transformation of behavior, cognitive abilities and other functions of the central nervous system in stress-sensitive individuals. Currently, it has been proven that in the pathogenesis of PTSD, an important place is occupied by changes in the number and composition of the intestinal microbiota. In this regard, methods of improving the microflora are being considered. Analyzing data of Russian and foreign researchers, the authors came to the conclusion, that metabolic, somatic and mental health largely depends on the coordinated functioning of the main interdependent components of metabolism: hepatobiliary system, intestinal microbiota and, according to the authors, on the state of mast cells. A close study of the interaction of these components will allow us to identify new therapeutic targets and the most effective methods of treating PTSD.

Dose-dependent effect of acute THC on extinction memory recall and fear renewal: a randomized, double-blind, placebo-controlled study.

Prior work from our lab and others demonstrates that the endocannabinoid system is a promising avenue for improving fear memory deficits in posttraumatic stress disorder (PTSD). Specifically, 7.5mg of delta-9-tetrahydrocannabinol (THC) decreases fear responding in healthy adults and increases prefrontal cortex activation during extinction learning and fear renewal in adults with PTSD. The present study will determine whether there is a dose-dependent effect of THC on short-term (24h) and long-term (one week) fear learning and memory in adults with PTSD. Using a randomized, double-blind, placebo-controlled design, N = 36 adults with PTSD completed the study and were randomized to receive placebo (PBO, n = 11), 5mg of THC (n = 11), or 10mg of THC (n = 14) prior to fear extinction learning. Participants completed a Pavlovian conditioning paradigm with extinction recall and fear renewal occurring 24h and one week later, where we measured concurrent functional imaging and behavioral responses. Twenty-four hours after drug administration, individuals with PTSD given 5mg of THC exhibited greater anterior cingulate cortex and prefrontal cortex activation during early fear renewal. One week later, individuals given 10mg of THC exhibited greater hippocampus activation during extinction recall and prefrontal cortex activation during fear renewal. These data suggest that dosing and timing are critical for facilitating fear memory processes in PTSD, and that low-dose oral THC prior to extinction learning can affect brain indices of fear learning and memory both acutely and one week after administration.

Self-construal modulates default mode network connectivity in refugees with PTSD

BackgroundWhile self-construal and posttraumatic stress disorder (PTSD) are independently associated with altered self-referential processes and underlying default mode network (DMN) functioning, no study has examined how self-construal affects DMN connectivity in PTSD. MethodsA final sample of 93 refugee participants (48 with DSM-5 PTSD or sub-syndromal PTSD and 45 matched trauma-exposed controls) completed a 5-minute resting state fMRI scan to enable the observation of connectivity in the DMN and other core networks. A self-construal index was calculated by substracting scores on the collectivistic and individualistic sub-scales of the Self Construal Scale. ResultsIndependent components analysis identified 9 active networks-of-interest, and functional network connectivity was determined. A significant interaction effect between PTSD and self-construal index was observed in the anterior ventromedial DMN, with spatial maps localizing this to the left ventromedial prefrontal cortex (vmPFC), extending to the ventral anterior cingulate cortex. This effect revealed that connectivity in the vMPFC showed greater reductions in those with PTSD with higher levels of collectivistic self-construal. LimitationsThis is an observational study and causality cannot be assumed. The specialized sample of refugees means that the findings may not generalize to other trauma-exposed populations. ConclusionsSuch a finding indicates that self-construal may shape the core neural architecture of PTSD, given that functional disruptions to the vmPFC underpin the core mechanisms of extinction learning, emotion dysregulation and self-referential processing in PTSD. Results have important implications for understanding the universality of neural disturbances in PTSD, and suggest that self-construal could be an important consideration in the assessment and treatment of post-traumatic stress reactions.

The Synergistic Trio of Metabolic Master Regulators Sustaining a Vicious Circle of Pathological Processes in Post-Traumatic Stress Disorder

Post-traumatic stress disorder (PTSD) is a maladaptive responseto the exposure of an extraordinary-intensity stressor. The animaland human body responds to any external challenges at the systemic, organismaland cellular levels. In stress-sensitive individuals, the collaborationof stress-implementing and stress-limiting systems is compromised,causing the transformation of behavior, cognitive abilities andother functions of the central nervous system. It is commonly acceptednow that changes in the abundance and repertoire of the intestinalmicrobiota play an important role in the pathogenesis of PTSD. Inthis regard, the methods of improving the microflora are high onthe agenda. Analyzing the literature data, we came to the conclusionthat metabolic, somatic and mental health largely depends on thecoordinated functioning of the key interdependent metabolic components:hepatobiliary system, intestinal microbiota and, as we believe,the state of mast cells. Close scrutiny of the interplay of these componentswill help identify new therapeutic targets and the most effectivemethods to treat PTSD.

Does disconfirmatory evidence shape safety-and danger-related beliefs of trauma-exposed individuals?

ABSTRACT Recent accounts of predictive processing in posttraumatic stress disorder (PTSD) suggest that trauma-exposed individuals struggle to update trauma-related hypotheses predicting danger, which may be involved in the etiology and maintenance of this disorder. Initial research supports this account, documenting an association between trauma-exposure, impaired expectation updating, and PTSD symptoms. Yet, no study to date has examined biased belief updating in PTSD using a scenario-based approach. Objective: Here, we examined the predictive processing account among trauma-exposed and non-trauma-exposed individuals using a modified Trauma-Related version of the Bias Against Disconfirmatory Evidence task. Method: The task presents both danger-and safety-related scenarios highly relevant for trauma-exposed individuals. For each scenario, participants viewed several explanations and rated their plausibility. Their ability to update their initial interpretation following new-contradictory information was assessed. Results: Preregistered analyses did not reveal any significant findings. Based on indications that our sample may not have been sufficiently powered, we conducted exploratory analyses in an extended sample of participants. These analyses yielded a significant association between reduced belief updating and PTSD symptoms which was evident for disconfirming both safety and danger scenarios. However, the effect sizes we found were in the small-to-medium range. Conclusion: Although preliminary, our current findings support initial evidence that individuals with higher PTSD symptoms show a higher resistance to update their beliefs upon new disconfirmatory evidence. Our results should be interpreted cautiously in light of the extended sample and the limitations of the current study.

Inflammation in Posttraumatic Stress Disorder: Dysregulation or Recalibration?

Despite ample experimental data indicating a role of inflammatory mediators in the behavioral and neurobiological manifestations elicited by exposure to physical and psychologic stressors, causative associations between systemic low-grade inflammation and central nervous system inflammatory processes in posttraumatic stress disorder (PTSD) patients remain largely conceptual. As in other stress-related disorders, pro-inflammatory activity may play an equivocal role in PTSD pathophysiology, one that renders indiscriminate employment of anti-inflammatory agents of questionable relevance. In fact, as several pieces of preclinical and clinical research convergingly suggest, timely and targeted potentiation rather than inhibition of inflammatory responses may actually be beneficial in patients who are characterized by suppressed microglia function in the face of systemic low-grade inflammation. The deleterious impact of chronic stress-associated inflammation on the systemic level may, thus, need to be held in context with the - often not readily apparent - adaptive payoffs of low-grade inflammation at the tissue level.

The neural circuits and molecular mechanisms underlying fear dysregulation in posttraumatic stress disorder.

Post-traumatic stress disorder (PTSD) is a stress-associated complex and debilitating psychiatric disorder due to an imbalance of neurotransmitters in response to traumatic events or fear. PTSD is characterized by re-experiencing, avoidance behavior, hyperarousal, negative emotions, insomnia, personality changes, and memory problems following exposure to severe trauma. However, the biological mechanisms and symptomatology underlying this disorder are still largely unknown or poorly understood. Considerable evidence shows that PTSD results from a dysfunction in highly conserved brain systems involved in regulating stress, anxiety, fear, and reward circuitry. This review provides a contemporary update about PTSD, including new data from the clinical and preclinical literature on stress, PTSD, and fear memory consolidation and extinction processes. First, we present an overview of well-established laboratory models of PTSD and discuss their clinical translational value for finding various treatments for PTSD. We then highlight the research progress on the neural circuits of fear and extinction-related behavior, including the prefrontal cortex, hippocampus, and amygdala. We further describe different molecular mechanisms, including GABAergic, glutamatergic, cholinergic, and neurotropic signaling, responsible for the structural and functional changes during fear acquisition and fear extinction processes in PTSD.

Adenosine A2A receptors control generalization of contextual fear in rats

Fear learning is essential to survival, but traumatic events may lead to abnormal fear consolidation and overgeneralization, triggering fear responses in safe environments, as occurs in post-traumatic stress disorder (PTSD). Adenosine A2A receptors (A2AR) control emotional memory and fear conditioning, but it is not known if they affect the consolidation and generalization of fear, which was now investigated. We now report that A2AR blockade through systemic administration of the A2AR antagonist SCH58261 immediately after contextual fear conditioning (within the consolidation window), accelerated fear generalization. Conversely, A2AR activation with CGS21680 decreased fear generalization. Ex vivo electrophysiological recordings of field excitatory post-synaptic potentials (fEPSPs) in CA3-CA1 synapses and of population spikes in the lateral amygdala (LA), showed that the effect of SCH58261 is associated with a reversion of fear conditioning-induced decrease of long-term potentiation (LTP) in the dorsal hippocampus (DH) and with increased amplitude of LA LTP in conditioned animals. These data suggest that A2AR are engaged during contextual fear consolidation, controlling long-term potentiation mechanisms in both DH and LA during fear consolidation, impacting on fear generalization; this supports targeting A2AR during fear consolidation to control aberrant fear processing in PTSD and other fear-related disorders.

Time course of attentional bias and its relationship with PTSD symptoms in bereaved Chinese parents who have lost their only child

ABSTRACT Background: The death of a child is a highly traumatic event for parents and often leads to posttraumatic stress disorder (PTSD). Attentional bias has been demonstrated in the onset and maintenance of PTSD symptoms. Objective: This study aimed to investigate the time course of attentional bias among bereaved Chinese parents who have lost their only child (Shidu parents), and to examine its relationship with PTSD symptoms and symptom clusters. Methods: Shidu parents (n = 38; 50–72 years of age) completed a dot-probe task with negative (trauma-related), positive, and neutral images at four stimulus presentation times (250, 500, 750, and 1250 ms). PTSD symptoms were measured by the PTSD Checklist for DSM-5 (PCL-5). Results: We observed difficulty in disengaging from both negative and positive stimuli at 750 ms and attentional bias away from negative stimuli at 1250 ms. At 1250 ms, attentional avoidance of trauma-related stimuli was positively correlated with PCL-5 total and intrusion scores. Difficulty in disengaging from positive stimuli was negatively correlated with PCL-5 total and intrusion scores as well as negative alterations in cogniti and mood scores. Conclusions: These findings enhance our understanding of attentional bias and cognitive–affective processing in PTSD. This study provides evidence that attentional bias (difficulty in disengaging from positive stimuli and bias away from negative stimuli) are correlated with PTSD symptoms and certain symptom clusters.

Fear Extinction Learning in Posttraumatic Stress Disorder.

Impairments in fear extinction processes have been implicated in the genesis and maintenance of debilitating psychopathologies, including Posttraumatic stress disorder(PTSD). PTSD, classified as a trauma- and stressor-related disorder, is characterized by four symptom clusters: intrusive recollections of trauma, avoidance of trauma-related stimuli, alterations in cognition and mood, and hyperarousal. One of the key pathological feature associated with the persistence of these symptoms is impaired fear extinction, as delineated in multiple studies employing Pavlovian fear-conditioning paradigms. These paradigms, comprising fear acquisition, extinction, extinction recall, and fear renewal phases, have illuminated the neurobiological substrates of PTSD. Dysfunctions in the neural circuits that mediate these fear learning and extinction processes can result in failure to extinguish fear responses and retain extinction memory, giving rise to enduring experience of fear and anxiety. The protective avoidance behaviors observed in individuals with PTSD further exacerbate intrusive symptoms and pose challenges to effective treatment strategies. A comprehensive analysis of fear conditioning and extinction processes, along with the underlying neurobiology, could significantly enhance our understanding of PTSD pathophysiology. This chapter delineates the role of fear extinction processes in PTSD, investigates the underlying neurobiological substrates, and underscores the therapeutic implications, while also identifying future research directions.

Scene Construction and Spatial Processing in Post-traumatic Stress Disorder.

IntroductionPost-traumatic stress disorder (PTSD) is associated with hippocampal system structural and functional impairments. Neurobiological models of PTSD posit that contextual memory for traumatic events is impaired due to hippocampal system dysfunction whilst memory of sensory details is enhanced due to amygdalar impact on sensory cortices. If hippocampal system dysfunction is a core feature of PTSD, then non-traumatic hippocampal-dependent cognitive functions such as scene construction, spatial processing, and memory should also be impaired in individuals with PTSD.MethodsForty-six trauma survivors, half diagnosed with PTSD, performed two tasks that involved spatial processing. The first was a scene construction task which requires conjuring-up spatially coherent multimodal scenarios, completed by all participants. Twenty-six participants (PTSD: n = 13) also completed a navigation task in a virtual environment, and underwent structural T1, T2 and diffusion-tensor MRI to quantify gray and white matter integrity. We examined the relationship between spatial processing, neural integrity, and symptom severity in a multiple factor analysis.ResultsOverall, patients with PTSD showed impaired performance in both tasks compared to controls. Scenes imagined by patients were less vivid, less detailed, and generated less sense of presence; importantly they had disproportionally reduced spatial coherence between details. Patients also made more errors during virtual navigation. Two components of the multiple factor analysis captured group differences. The first component explained 25% of the shared variance: participants that constructed less spatially coherent scenes also made more navigation errors and had reduced white matter integrity to long association tracts and tracts connecting the hippocampus, thalamus, and cingulate. The second component explained 20% of the variance: participants who generated fewer scene details, with less spatial coherence between them, had smaller hippocampal, parahippocampal and isthmus cingulate volumes. These participants also had increased white matter integrity to the right hippocampal cingulum bundle.ConclusionOur results suggest that patients with PTSD are impaired at imagining even neutral spatially coherent scenes and navigating through a complex spatial environment. Patients that showed reduced spatial processing more broadly had reduced hippocampal systems volumes and abnormal white matter integrity to tracts implicated in multisensory integration.

P619. An Emotion Processing Function for N2 Sleep Spindles in Posttraumatic Stress Disorder

Sleep spindles, bursts of 11-16 Hz oscillatory rhythms, are a signature feature of non-REM (NREM) sleep and underlie information processing and memory consolidation. The role of spindles in emotional information processing in posttraumatic stress disorder (PTSD), characterized by disturbed sleep and traumatic memories, remains unknown.

Avoidance behaviour generalizes to eye processing in posttraumatic stress disorder

ABSTRACT Background Avoidance describes any action designed to prevent an uncomfortable situation or emotion from occurring. Although it is a common reaction to trauma, avoidance becomes problematic when it is the primary coping strategy, and plays a major role in the development and maintenance of posttraumatic stress disorder (PTSD). Avoidance in PTSD may generalize to non-harmful environmental cues that are perceived to be unsafe. Objective We tested whether avoidance extends to social cues (i.e. emotional gazes) that are unrelated to trauma. Method A total of 159 participants (103 who had been exposed to the 2015 Paris terrorist attacks and 56 who had not) performed a gaze-cueing task featuring sad, happy and neutral faces. Attention to the eye area was recorded using an eyetracker. Of the exposed participants, 52 had been diagnosed with PTSD (PTSD+) and 51 had not developed PTSD (PTSD-). As a result of the preprocessing stages, 52 PTSD+ (29 women), 50 PTSD- (20 women) and 53 nonexposed (31 women) participants were included in the final analyses. Results PTSD+ participants looked at sad eyes for significantly less time than PTSD- and nonexposed individuals. This effect was negatively correlated with the intensity of avoidance symptoms. No difference was found for neutral and happy faces. Conclusions These findings suggest that maladaptive avoidance in PTSD extends to social processing, in terms of eye contact and others’ emotions that are unrelated to trauma. New therapeutic directions could include targeting sociocognitive deficits. Our findings open up new and indirect avenues for overcoming maladaptive avoidance behaviours by remediating eye processing. Trial registration: ClinicalTrials.gov identifier: NCT02810197. HIGHLIGHTS Avoidance is a key symptom of posttraumatic stress disorder (PTSD). Avoidance is often viewed as limited to reminders linked to the trauma. Results show that attention to the eyes of sad faces is also affected by PTSD. This effect is correlated with avoidance symptoms in PTSD

Examining Cultural Differences in the Associations between Appraisals and Emotion Regulation and PostTraumatic Stress Disorder in Malaysian and Australian Trauma Survivors.

Appraisals and emotional regulation play a central role in posttraumatic stress disorder (PTSD). Despite research demonstrating cultural differences in everyday appraisals and emotion regulation, little research has investigated the influence of culture on these processes in PTSD. This study examined cultural differences in the associations between appraisals, emotion regulation and PTSD symptoms using trauma survivors from an individualistic Western culture (Australia) and a collectivistic Asian culture (Malaysia). Trauma survivors (N = 228; 107 Australian with European cultural heritage, 121 Malaysian with Malay, Indian or Chinese cultural heritage) completed an on-line survey assessing PTSD (PTSD Checklist for the DSM-5 with Life Events Checklist), appraisals (trauma-related, fatalism, cultural beliefs about adversity) and emotion regulation (suppression, reappraisal, interpersonal). The Malaysian group reported significantly greater fatalism, cultural beliefs about adversity, suppression and interpersonal emotion regulation than the Australian group. Greater trauma-specific appraisals, greater suppression, fewer cultural beliefs about adversity, and less use of social skills to enhance positivity were generally associated with greater PTSD symptom severity, with little evidence of cultural group moderating these associations. Interdependent self-construal mediated the relationships between cultural adversity beliefs, enhanced positivity, reappraisal, perspective taking and PTSD symptoms. Independent self-construal mediated the relationships between fatalism and perspective taking and PTSD symptoms. Cultural group did not moderate these indirect effects. Interdependent self-construal mediated the associations between interpersonal regulation strategies of soothing and social modelling with PTSD symptoms for the Malaysian but not the Australian group. These findings demonstrate the importance of considering self-construal and culture in understanding factors associated with PTSD.

Differential Role of mGluR5 in Cognitive Processes in Posttraumatic Stress Disorder and Major Depression

Background A robust literature supports the role of the metabotropic glutamate receptor type 5 (mGluR5) in cognitive functioning. mGluR5 is also implicated in the pathophysiology of posttraumatic stress disorder (PTSD) and major depressive disorder (MDD), which are characterized by cognitive alterations. However, the relationship between mGluR5 and cognition in MDD and PTSD has not yet been directly investigated. To address this gap, we examined the relationship between in vivo mGluR5 availability and cognition in PTSD, MDD, and matched healthy adults (HA). Methods Individuals with PTSD (N = 28) and MDD (N = 21), and HA (N = 28) were matched for age, gender, and smoking status. Participants completed 18F-FPEB positron emission tomography (PET) scan, psychiatric and cognitive assessments. Results Across models examining the relationship between mGluR5 availability and different domains of cognition across diagnostic groups, only the interaction of diagnosis*attention was significant (F4,64 = 3.011, P = .024). Higher mGluR5 availability was associated with poorer attention in PTSD in 4 frontolimbic regions of interests (ROI's: OFC (r = −.441, P = .016), vmPFC (r = −.408, P = .028), dlPFC (r = −.421, P = .023), hippocampus (r = −.422, P = .025). By contrast, mGluR5 availability in the MDD group was positively related to Attention (ATTN) in the OFC (r = .590, P = .006), vmPFC (r = .653, P = .002), and dlPFC (r = .620, P = .004). Findings in the hippocampus for MDD followed the same pattern but did not survive correction for multiple comparisons (r = .480, P = .036). ATTN and mGluR5 availability were not significantly related in the HA group. Of note, in MANOVA analyses group*ATTN interaction results in the OFC did not survive multiple comparisons (P = .046). All other findings survived correction for multiple comparisons and remained significant when covarying for potential confounds (eg, depressed mood). Conclusions We observed a significant relationship between frontolimbic mGluR5 availability and performance on tests of attention in individuals with MDD and PTSD. This finding aligns with animal work showing dysregulation in mGluR5 in cognitive functioning, and differed as a function of diagnosis. Results suggest interventions targeting mGluR5 may help bolster cognitive difficulties, highlighting the importance of employing different mGluR5 directed treatment strategies in MDD and PTSD.

Punishment and reward normalize error-related cognitive control in PTSD by modulating salience network activation and connectivity

Posttraumatic Stress Disorder (PTSD) symptomatology disrupts inhibitory control during sustained attention. However, PTSD-related inhibitory control deficits are partially ameliorated when punishments and rewards are administered based on task performance, which suggests motivational processes contribute to these deficits. Additionally, PTSD may also impair error-related cognitive control following inhibitory control failures as measured by post-error slowing (PES). However, it remains unclear if motivational processes also contribute to impaired error-related cognitive control in PTSD. Using an incentivized sustained attention paradigm in two independent samples of post-9/11 veterans, we characterized PTSD-related differences in PES during both non-motivated conditions (no task-based incentives) and motivated conditions (task-based rewards and punishments). In Study 1 (n = 139), PTSD symptom severity was modestly associated with smaller PES in the non-motivated condition, whereas no PTSD-related association was observed in the motivated condition. In Study 2 (n = 35), we replicated and extended these results by using fMRI to characterize modulation of the triple network system comprised of the Salience Network (SN), Frontoparietal Control Network (FPCN), and Default Mode Network (DMN). In the non-motivated condition, PTSD symptom severity was associated with non-specific SN and FPCN hyperactivation during both failed and successful inhibitory control. In the motivated condition, PTSD symptom severity was associated with greater focal activation of both the SN and Superior Parietal Lobule cluster (an FPCN node) during punished inhibitory control failures and weaker SN-FPCN connectivity during rewarded inhibitory control successes. Together, these results suggest that dysregulated motivational processes in PTSD may contribute to impaired error-related cognitive control.

Anhedonia in PTSD is Related to Higher Right Anterior Insula Glutamate and Accelerated Delay Discounting: A Magnetic Resonance Spectroscopy Study

In posttraumatic stress disorder (PTSD), the anterior insula (AI) is hyperresponsive to trauma cues and negative emotions. Recent research suggests that the AI exerts inhibitory control over reward circuitry including the nucleus accumbens. We are unaware of prior reports of the role of glutamatergic activity in the AI on reward processing in PTSD. We hypothesized that elevated right AI glutamate would be associated with anhedonia and faster devaluation of delayed rewards (accelerated delay discounting).

The sense of self in the aftermath of trauma: lessons from the default mode network in posttraumatic stress disorder

ABSTRACT Trauma can profoundly affect the sense of self, where both cognitive and somatic disturbances to the sense of self are reported clinically by individuals with posttraumatic stress disorder (PTSD). These disturbances are captured eloquently by clinical accounts, such as, ‘I do not know myself anymore,’ ‘I will never be able to experience normal emotions again,’ and, ‘I feel dead inside.’ Self-related thoughts and experiences are represented neurobiologically by a large-scale, cortical network located along the brain’s mid-line and referred to as the default mode network (DMN). Recruited predominantly during rest in healthy participants, the DMN is also active during self-referential and autobiographical memory processing – processes which, collectively, are thought to provide the foundation for a stable sense of self that persists across time and may be available for conscious access. In participants with PTSD, however, the DMN shows substantially reduced resting-state functional connectivity as compared to healthy individuals, with greater reductions associated with heightened PTSD symptom severity. Critically, individuals with PTSD describe frequently that their traumatic experiences have become intimately linked to their perceived sense of self, a perception which may be mediated, in part, by alterations in the DMN. Accordingly, identification of alterations in the functional connectivity of the DMN during rest, and during subliminal, trauma-related stimulus conditions, has the potential to offer critical insight into the dynamic interplay between trauma- and self-related processing in PTSD. Here, we discuss DMN-related alterations during these conditions, pointing further towards the clinical significance of these findings in relation to past- and present-centred therapies for the treatment of PTSD.

Pupillary Response to Affective Voices: Physiological Responsivity and Posttraumatic Stress Disorder.

Posttraumatic stress disorder (PTSD) is related to dysfunctional emotional processing, thus motivating the search for physiological indices that can elucidate this process. Toward this aim, we compared pupillary response patterns in response to angry and fearful auditory stimuli among 99 adults, some with PTSD (n = 14), some trauma-exposed without PTSD (TE; n = 53), and some with no history of trauma exposure (CON; n = 32). We hypothesized that individuals with PTSD would show more pupillary response to angry and fearful auditory stimuli compared to those in the TE and CON groups. Among participants who had experienced a traumatic event, we explored the association between PTSD symptoms and pupillary response; contrary to our prediction, individuals with PTSD displayed the least pupillary response to fearful auditory stimuli compared those in the TE, B = -0.022, p = .077, and CON, B = -0.042, p = .002, groups, but they did not differ on angry auditory stimuli, B = 0.019, p = .118 and B = 0.006, p = .634, respectively. It is important to note that within-group analyses revealed that participants with PTSD differed significantly in their response to angry versus fearful stimuli, B = -0.032, p = .015. We also found a positive association between PTSD symptoms and pupillary response to angry stimuli. Our findings suggest that differential pupil response to anger and fear stimuli may be a promising way to understand emotional processing in PTSD.

Acute Posttraumatic Symptoms Are Associated With Multimodal Neuroimaging Structural Covariance Patterns: A Possible Role for the Neural Substrates of Visual Processing in Posttraumatic Stress Disorder

BackgroundAlthough aspects of brain morphology have been associated with chronic posttraumatic stress disorder (PTSD), limited work has investigated multimodal patterns in brain morphology that are linked to acute posttraumatic stress severity. In the present study, we utilized multimodal magnetic resonance imaging to investigate if structural covariance networks (SCNs) assessed acutely following trauma were linked to acute posttraumatic stress severity. MethodsStructural magnetic resonance imaging data were collected around 1 month after civilian trauma exposure in 78 participants. Multimodal magnetic resonance imaging data fusion was completed to identify combinations of SCNs, termed structural covariance profiles (SCPs), related to acute posttraumatic stress severity collected at 1 month. Analyses assessed the relationship between participant SCP loadings, acute posttraumatic stress severity, the change in posttraumatic stress severity from 1 to 12 months, and depressive symptoms. ResultsWe identified an SCP that reflected greater gray matter properties of the anterior temporal lobe, fusiform face area, and visual cortex (i.e., the ventral visual stream) that varied curvilinearly with acute posttraumatic stress severity and the change in PTSD symptom severity from 1 to 12 months. The SCP was not associated with depressive symptoms. ConclusionsWe identified combinations of multimodal SCNs that are related to variability in PTSD symptoms in the early aftermath of trauma. The identified SCNs may reflect patterns of neuroanatomical organization that provide unique insight into acute posttraumatic stress. Furthermore, these multimodal SCNs may be potential candidates for neural markers of susceptibility to both acute posttraumatic stress and the future development of PTSD.