Posttraumatic Stress Disorder or Combat Experience? A Functional Near-infrared Spectroscopy Study of Trauma-related Auditory and Olfactory Cues

While the clinical communities are aware of the prevalence of posttraumatic stress disorder (PTSD) among OEF/OIF/OND veterans, further efforts are necessary to bolster comprehensive strategies for assessment and treatment. The purpose of this study was to investigate whether a combat-related PTSD symptom provocation paradigm would elicit unique neurological responses via functional near-infrared spectroscopy across three groups – combat veterans with PTSD, combat veterans without PTSD, and nonmilitary participants without PTSD. Results indicated that combat veterans with PTSD demonstrated significant activation during exposure to a trauma-related sound compared to nonmilitary personnel at channels 14 (d = 1.03) and 15 (d = 1.30) and combat veterans without PTSD at channel 14 (d = 0.87). Specifically, this increased neural activation was approximately located in the right superior/medial prefrontal cortex (BA 9/10), associated with evaluating cue-familiarity and emotional detachment. Results were less clear with respect to a combat-related odor. These results suggest a specific neurophysiological response to trauma-related cues and if replicated, may offer a biomarker for combat-related PTSD. Such a response could provide incremental validity over diagnostic assessments alone and assist in planning and monitoring of treatment outcome

Traumatic Brain Injury Service, Walter Reed National Military Medical Center 4. National Intrepid Center of Excellence, Walter Reed National Military Medical Center 5. National Institute of Nursing Research , National Institutes of Health 6. RTI Internati

Abstract Traumatic brain injury, depression and posttraumatic stress disorder (PTSD) are neurocognitive syndromes often associated with impairment of physical and mental health, as well as functional status. These syndromes are also frequent in military service members (SMs) after combat, although their presentation is often delayed until months after their return. The objective of this prospective cohort study was the identification of independent predictors of neurocognitive syndromes upon return from deployment could facilitate early intervention to prevent disability. We completed a comprehensive baseline assessment, followed by serial evaluations at three, six, and 12 months, to assess for new-onset PTSD, depression, or postconcussive syndrome (PCS) in order to identify baseline factors most strongly associated with subsequent neurocognitive syndromes. On serial follow-up, seven participants developed at least one neurocognitive syndrome: five with PTSD, one with depression and PTSD, and one with PCS. On univariate analysis, 60 items were associated with syndrome development at p < 0.15. Decision trees and ensemble tree multivariate models yielded four common independent predictors of PTSD: right superior longitudinal fasciculus tract volume on MRI; resting state connectivity between the right amygdala and left superior temporal gyrus (BA41/42) on functional MRI; and single nucleotide polymorphisms in the genes coding for myelin basic protein as well as brain-derived neurotrophic factor. Our findings require follow-up studies with greater sample size and suggest that neuroimaging and molecular biomarkers may help distinguish those at high risk for post-deployment neurocognitive syndromes

Traumatic Brain Injury Service, Walter Reed National Military Medical Center 4. National Intrepid Center of Excellence, Walter Reed National Military Medical Center 5. National Institute of Nursing Research , National Institutes of Health 6. RTI Internati

Abstract Traumatic brain injury, depression and posttraumatic stress disorder (PTSD) are neurocognitive syndromes often associated with impairment of physical and mental health, as well as functional status. These syndromes are also frequent in military service members (SMs) after combat, although their presentation is often delayed until months after their return. The objective of this prospective cohort study was the identification of independent predictors of neurocognitive syndromes upon return from deployment could facilitate early intervention to prevent disability. We completed a comprehensive baseline assessment, followed by serial evaluations at three, six, and 12 months, to assess for new-onset PTSD, depression, or postconcussive syndrome (PCS) in order to identify baseline factors most strongly associated with subsequent neurocognitive syndromes. On serial follow-up, seven participants developed at least one neurocognitive syndrome: five with PTSD, one with depression and PTSD, and one with PCS. On univariate analysis, 60 items were associated with syndrome development at p < 0.15. Decision trees and ensemble tree multivariate models yielded four common independent predictors of PTSD: right superior longitudinal fasciculus tract volume on MRI; resting state connectivity between the right amygdala and left superior temporal gyrus (BA41/42) on functional MRI; and single nucleotide polymorphisms in the genes coding for myelin basic protein as well as brain-derived neurotrophic factor. Our findings require follow-up studies with greater sample size and suggest that neuroimaging and molecular biomarkers may help distinguish those at high risk for post-deployment neurocognitive syndromes

An Experimental Test of the Effects of Social Conflict on Posttraumatic Stress Symptoms and Alcohol Craving

While substantial efforts have been devoted to understanding links between posttraumatic stress disorder (PTSD) and hazardous alcohol use, relatively little research has examined possible third factor variables that may maintain this comorbidity. Social conflict is common among people suffering from posttraumatic stress symptoms (PTSS), hazardous alcohol use, and the combination of these two conditions, and is thought to maintain both PTSS and hazardous alcohol use. Fortunately, social conflict is malleable, but there is little evidence to date examining social conflict as a common maintaining factor. The current study investigated the effect of social conflict on state PTSS, alcohol craving, and alcohol approach bias in an effort to isolate one portion of a complex constellation of difficulties. A total of 46 participants with a history of trauma exposure and current hazardous alcohol use completed a laboratory-based assessment of posttraumatic stress symptom reactions, alcohol craving, and alcohol approach bias in response to social conflict, as manipulated via the script-driven imagery procedure. Results demonstrated that social conflict, compared to a neutral social script, elicited an increase in state PTSS symptoms, but not in alcohol craving, or alcohol approach bias. Sex was not demonstrated to have a moderating effect on social conflict as it relates to PTSS, alcohol craving, or alcohol approach bias. These findings highlight the role of social conflict in eliciting state PTSS; however, contrary to hypotheses social conflict did not elicit alcohol craving or approach bias. Possible reasons for these findings as well as limitations and future directions are discussed

PTSD and Dysfunctional Parenting: Emotional and Biological Mechanisms

Women are disproportionately at risk for developing PTSD following exposure to trauma. Among its many harmful effects, PTSD is associated with a range of negative family outcomes, including impairments in parenting behaviors. Despite the prevalence of PTSD and its impact on parenting, little is known about the mechanisms responsible for this association. The present project addressed this gap by examining the impact of PTSD on dysfunctional parenting behaviors in a lab setting. Based on prior theory and empirical evidence, I expected that a diagnosis of PTSD would be associated with more dysfunctional parenting (i.e., harsh/overreactive and lax/permissive behaviors) during routine mother-child discipline encounters. Further, drawing on research linking negative emotion and greater cortisol dysregulation to both PTSD and dysfunctional parenting, I expected emotional and physiological reactivity to mediate the relation between PTSD status and parenting behaviors. To test these hypotheses, 78 mothers and their 18- to 36-month-old children completed a task designed to elicit parental responses to typical instances of child misbehavior. Mothers then viewed a video of the interaction and provided in-the-moment ratings of their experienced emotions. Salivary cortisol was collected from mothers prior and subsequent to the lab paradigm to assess stress-related cortisol reactivity. PTSD diagnosis was assessed via the CAPS-5 interview. Findings revealed that mothers with PTSD were more likely to engage in lax parenting behaviors during the discipline encounter. Contrary to hypotheses, PTSD status was not significantly associated with overreactive parenting behaviors, and negative emotion and cortisol reactivity did not mediate relations between PTSD and dysfunctional parenting, when controlling for important covariates. Findings suggest that PTSD symptoms might increase mothers’ tendency to avoid making effortful attempts to manage child misbehavior during challenging parent-child interactions. Mothers with PTSD might benefit from interventions that help them set consistent limits in the context of everyday discipline encounters with their children. Advisor: David DiLill

ADVANCING THE MEASUREMENT OF TRAUMA-RELATED SHAME AMONG WOMEN WITH HISTORIES OF INTERPERSONAL VIOLENCE

Shame is a predominant emotion for some trauma-exposed individuals—particularly survivors of interpersonal violence (IPV)—that is associated with more severe symptoms of posttraumatic stress disorder (PTSD; see Saraiya & Lopez-Castro, 2016). Despite growing evidence of shame’s importance in recovery from trauma and PTSD, measurement challenges have played a large role in difficulties understanding and comparing the impact of shame across studies. These challenges include: 1) the use of measures that assess trait shame as opposed to trauma-related shame, 2) inconsistent use of established shame measures across studies, and 3) failure to acknowledge the co-occurrence of shame and guilt. These limitations are notable, given that trauma-related shame appears to be more predictive of PTSD symptoms and other psychiatric difficulties than trait shame (Semb et al., 2011) and more predictive of PTSD symptoms than trauma-related guilt (Cunningham et al., 2018). The Trauma-Related Shame Inventory (TRSI; Øktedalen et al., 2014) is the most widely used measure of trauma-related shame, yet additional psychometric support is needed. Two studies were thus conducted to provide additional psychometric validation to support the use of the TRSI among women with IPV histories and to better understand how trauma-related shame, relative to trait shame and trauma-related guilt, are associated with PTSD symptoms among this population

Heart Rate Variability Following Treatment for PTSD: Testing the Polyvagal Theory

Posttraumatic stress disorder (PTSD) has been linked to lower heart rate variability (HRV), including measures of vagal tone. Treatments targeting the autonomic nervous system (ANS) have demonstrated efficacy in improving vagal tone, but it is less clear whether similar effects can also be achieved with cognitive therapies. The polyvagal theory has suggested that symptoms of social dysfunction are linked to vagal tone through a phylogenetically organized response to stress. HRV was collected during rest, reactivity (exposure to personalized trauma scripts), and recovery using a scripted imagery paradigm in female PTSD positive physical and sexual assault survivors (N = 41) prior to and following completion of cognitive processing therapy (CPT). Effects of treatment response and a supplementary sleep-directed hypnosis treatment were also assessed. To test the premise that vagal tone is related to social functioning, regressions predicting scores on Social Adjustment Scale (SAS) with high frequency (HF) HRV were completed. Vagal tone during trauma cue exposure improved following CPT, but only in treatment responders; during all other assessment periods it decreased posttreatment and there was no effect of treatment response. However, including depression symptoms as a covariate rendered all previously significant effects non-significant. The supplementary treatment had no effect on HRV during any of the measurement periods. Findings indicate the potential for cognitive therapies to impact vagal tone, despite not directly targeting the ANS. Minimal support for the polyvagal theory was found in the extended family subscale of the SAS, which was the only domain to demonstrate a significant relationship to vagal tone

EEG Asymmetries in Survivors of Severe Motor Accidents: Association with Posttraumatic Stress Disorder and its Treatment as well as Posttraumatic Growth: EEG Asymmetries in Survivors of Severe Motor Accidents: Association with Posttraumatic Stress Disorder and its Treatment as well as Posttraumatic Growth

Severe motor vehicle accidents (MVAs) represent one of the most often occurring psychological traumas, and are a leading cause of Posttraumatic Stress Disorder (PTSD). However, not all persons develop PTSD after traumatic events and a great proportion of patients who show symptoms initially recover over time. This has stimulated research of psychological and biological factors that explain development and maintenance of the disorder. Fortunately, this highly distressing condition can be effectively treated, e.g. via cognitive behavioral therapy (CBT). However, brain mechanisms underlying changes due to psychological therapy in PTSD are almost unknown (Roffman, Marci, Glick, Dougherty, & Rauch, 2005). On the other hand there are observations of positive changes following trauma called Posttraumatic Growth (PTG), which have stimulated research of associated psychological processes and factors. However, there is a lack of research about the relation of biological variables (e.g. measures of brain function) and PTG. Theories of brain asymmetry and emotion (Davidson, 1998b, 2004b; Heller, Koven, & Miller, 2003) propose that asymmetries of brain activation are related to certain features of human emotion (e.g. valence, approach or withdrawal tendencies, arousal). Whereas an enormous increase in the understanding of structural and functional abnormalities in PTSD could be achieved in the last decades due to neuroimaging research, there are still numerous unanswered questions. Especially, there is only little research explicitly examining activation asymmetries in PTSD. Furthermore, as mentioned, research is sparse investigating alterations of brain function that are associated with successful psychological treatment of PTSD. Finally, there is no published study examining how measures of brain function are related to PTG. This thesis presents 3 studies investigating electroencephalographic (EEG) asymmetries in survivors of severe motor vehicle accidents. The first part of the thesis (chapter 2) is devoted to a literature review about description (chapter 2.1), epidemiology (chapter 2.2 and 2.3), risk factors (chapter 2.4), psychological theories (chapter 2.5), biological mechanisms particularly neuroimaging findings (chapter 2.6), and treatment of PTSD (chapter 2.7.). Chapter 2.8 gives a short review on definition and research of Posttraumatic Growth. Chapter 2.9 provides an overview of models and research regarding brain asymmetry and emotion. In chapter 3.1, a study is presented that investigated hemispheric asymmetries (EEG alpha) among MVA survivors with PTSD, with subsyndromal PTSD, and without PTSD as well as non-exposed healthy controls during a baseline condition and in response to neutral, positive, negative, and trauma-related pictures (study I). Next, the findings of study II are presented (chapter 3.2). This study examined the effect of cognitive behavioral therapy on measures of EEG activity. Therefore, EEG activity before and after CBT in comparison to an assessment only Wait-list condition was measured. In chapter 3.3 a correlational study (study III) is presented that examined the relationship between frontal brain asymmetry and selfreported posttraumatic growth after severe MVAs. Finally, in chapter 4 the findings are summarized and discussed with respect to (1) the state/trait debate in frontal asymmetry research and (2) current psychological theories of PTSD and PTG. In addition, the use of neuroscientific research for psychotherapy is discussed. Suggestions are presented for future goals for “brain” research of PTSD and treatment of PTSD.Schwere Verkehrsunfälle stellen eines der am häufigsten vorkommenden psychologischen Traumata dar, und sind eine Hauptursache der Posttraumatischen Belastungsstörung (PTBS). Jedoch entwickeln nicht alle Personen nach traumatischen Ereignissen eine PTBS und bei einem Großteil remittieren anfängliche PTBS-Symptome. Dies stimulierte die Erforschung von psychologischen und biologischen Faktoren, die die Entstehung und Aufrechterhaltung der PTBS erklären. Glücklicherweise kann die PTBS effektiv, z.B über die kognitive Verhaltenstherapie (KVT), behandelt werden. Jedoch sind Gehirnmechanismen, die mit klinischen Änderungen aufgrund der psychologischen Therapie in PTSD einhergehen, nahezu unbekannt (Roffman, Marci, Glick, Dougherty, Rauch, 2005). Auf der anderen Seite gibt es Berichte von positiven Änderungen nach traumatischen Ereignissen, die als Posttraumatische Reifung (PTR) bezeichent werden. Dies hat in kürzerer Vergangenheit die Forschung von verbundenen psychologischen Prozessen und Faktoren stimuliert. Jedoch gibt es kaum Untersuchungen über die Beziehung von biologischen Variablen (z.B Messungen der Gehirnfunktion) und PTR. Diese Arbeit präsentiert 3 Studien, die electroenzephalographische (EEG) Asymmetrien bei Opfern schwerer Verkehrsunfälle untersuchten. Der erste Teil der Arbeit (Kapitel 2) widmet sich einer Literaturrezension über: die Beschreibung (Kapitel 2.1), Epidemiologie (Kapitel 2.2 und 2.3), Risikofaktoren (Kapitel 2.4), psychologische Theorien (Kapitel 2.5), biologische Mechanismen besonders Neuroimaging Ergebnisse (Kapitel 2.6), und Behandlung der PTBS (Kapitel 2.7.). Kapitel 2.8 gibt einen kurzen Überblick über die Definition und Forschung zur Posttraumatischen Reifung. Kapitel 2.9 gibt eine Übersicht zu aktuellen Modellen und empirischen Befunden bezüglich Gehirnasymmetrien und Emotionen. Kapitel 3.1 präsentiert eine Studie, in der hemisphärische Asymmetrien (im EEG-Alpha Band) bei Unfallopfern mit PTBS, subsyndromaler PTBS, und ohne PTBS sowie gesunden Kontrollpersonen ohne Unfall untersucht wurden: während einer Ruhemessung und einer Emotionsinduktions-bedingung (neutrale, positive, negative und trauma-spezifische Bilder) (Studie I). Danach werden die Ergebnisse der Studie II (Kapitel 3.2) präsentiert. Hier wurde die Wirkung der kognitiven Verhaltenstherapie auf Messungen der EEG-Aktivität untersucht. Deshalb wurde EEG-Aktivität vor und nach einer KVT im Vergleich mit einer Warten-Gruppe gemessen. Kapitel 3.3 präsentiert eine Korellationsanalyse (Studie III), bei der die Beziehung zwischen der frontalen Gehirnasymmetrie und posttraumatischer Reifung untersucht wurde. Am Ende der Arbeit (Kapitel 4) werden die Ergebnisse zusammengefasst und in Bezug auf (1) die state/trait-Debatte im Rahmen der Asymmetrie-Forschung diskutiert sowie (2) ein Bezug zu aktuellen psychologische Theorien von PTSD und PTG hergestellt. Außerdem wird der Nutzen von neurobiologischer Forschung für die Psychotherapie besprochen. Dabei werden Vorschläge für zukünftige Projekte für die "Gehirn"-Forschung im Zusammenhang mit der PTBS, deren Behandlung und PTG gemacht

Posttraumatic Stress Disorder: A Theoretical Model of the Hyperarousal Subtype

Posttraumatic stress disorder (PTSD) is a frequent and distressing mental disorder, about which much remains to be learned. It is a heterogeneous disorder; the hyperarousal subtype (about 70% of occurrences and simply termed PTSD in this paper) is the topic of this article, but the dissociative subtype (about 30% of occurrences and likely involving quite different brain mechanisms) is outside its scope. A theoretical model is presented that integrates neuroscience data on diverse brain regions known to be involved in PTSD, and extensive psychiatric findings on the disorder. Specifically, the amygdala is a multifunctional brain region that is crucial to PTSD, and processes peritraumatic hyperarousal on grounded cognition principles to produce hyperarousal symptoms. Amygdala activity also modulates hippocampal function, which is supported by a large body of evidence, and likewise amygdala activity modulates several brainstem regions, visual cortex, rostral anterior cingulate cortex (rACC), and medial orbitofrontal cortex (mOFC), to produce diverse startle, visual, memory, numbing, anger, and recklessness symptoms. Additional brain regions process other aspects of peritraumatic responses to produce further symptoms. These contentions are supported by neuroimaging, neuropsychological, neuroanatomical, physiological, cognitive, and behavioral evidence. Collectively, the model offers an account of how responses at the time of trauma are transformed into an extensive array of the 20 PTSD symptoms that are specified in the Diagnostic and Statistical Manual of Mental Disorders, 5th edition. It elucidates the neural mechanisms of a specific form of psychopathology, and accords with the Research Domain Criteria framewor

The Relationship Between Trauma Exposure, Somatic Symptoms, and Mental Health in Australian Defence Force Members Deployed to the Middle East Area of Operations

There is an increase in the prevalence of physical symptoms in military veterans who have deployed to combat zones compared to those who have not been deployed. These symptoms can be distressing, disabling, and negatively impact quality of life. Current paradigms regarding the effects of traumatic deployment exposures on military personnel tend to consider non-specific physical symptoms (that are not due to injury) as simply a comorbidity of psychological disorder following trauma, rather than independent sequelae. For example, the diagnostic criteria for a condition specifically caused by traumatic exposures, posttraumatic stress disorder (PTSD), do not include physical symptoms. Uncertainty surrounding the aetiology of physical symptoms has led to some fierce controversies, such as the existence of Gulf War Syndrome. The aim of this thesis was to examine how physical and psychological symptoms occur independently as well as co-occur in veterans post-deployment, and to examine the strength of associations between traumatic deployment exposures (TDEs) and these profiles of physical and psychological symptom presentation. A further aim was to explore how well a checklist of physical symptoms could identify concurrent PTSD. The final aim was to examine whether inflammation mediated associations between TDEs and physical symptoms. Data used in this thesis were from several related studies of Australian Defence Force (ADF) members who deployed to the Middle East Area of Operations (MEAO) from 2001 to 2012. These studies were commissioned by the Australian Government’s Department of Defence to explore the impact of increased operational tempo on the health of military personnel. These large-scale correlational studies surveyed tens of thousands of personnel using self-reported questionnaires which included gold-standard measures of psychological distress and PTSD, as well as checklists of trauma exposure and physical symptoms. This thesis substantiated prior findings of high rates of comorbidity between PTSD and physical symptoms in veterans. While results confirmed that physical and psychological symptoms can co-occur, analyses identified a subgroup of veterans who exhibited physical symptoms without psychological distress; this ‘physical only’ presentation was as common as the ‘psychological only’ and comorbid symptom presentations. Moreover, this presentation was associated with lower quality of life, and as such is worthy of clinical attention. Importantly, TDEs showed similar associations with both ‘physical only’ and ‘psychological only’ symptom presentations. As with First Gulf War research, there did not appear to be a particular post-deployment physical ‘syndrome’; while symptoms often co-occurred, it was symptom number and intensity rather than type that identified affected veterans. A list of 10 physical symptoms demonstrated good diagnostic utility for predicting cases of concurrent PTSD. The findings also suggest that sub-types of PTSD exist, differentiated by the level of somatic symptoms. While a relationship was found between some individual physical symptoms and inflammation, the hypothesis that inflammation mediates the relationship between trauma and physical symptoms was not supported. These findings validate physical symptoms as a discrete symptom outcome following deployment, and this presentation had a similar prevalence to co-occurring physical and psychological symptoms. Therefore, physical symptoms should not be regarded simply as a comorbidity of an underlying psychological disorder for all veterans. As physical symptoms are just as likely to occur as psychological symptoms following TDEs and they impact quality of life, they should be assessed during post-deployment screening and considered in civilian treatment of veterans. Furthermore, the inclusion of physical symptoms in PTSD screening checklists may improve PTSD identification rates and better describe the patient experience.Thesis (Ph.D.) -- University of Adelaide, Adelaide Medical School, 201