| Göhre, Isabelle (2026): Childhood trauma and psychopathology: investigating the role of social functioning, emotional processing, and sleep in Post-Traumatic Stress Disorder and Borderline Personality Disorder. Dissertation, LMU München: Fakultät für Psychologie und Pädagogik |
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Abstract
Traditional categorical systems provide useful diagnostic distinctions between mental disorders. However, they struggle to capture their high comorbidity, heterogeneity, and overlapping etiological pathways (Dalgleish et al., 2020). Consequently, a paradigm shift has been promoted toward dimensional and transdiagnostic frameworks that conceptualize psychopathology along a continuum of shared risk factors and mechanisms (Harvey et al., 2004). Within this perspective, traumatic childhood experiences (TCE) represent a key transdiagnostic risk factor for the development of various forms of psychopathology (Jaffee, 2017; Lewis et al., 2021; Walsh et al., 2017). TCE include emotional, physical, and sexual abuse and/or emotional and physical neglect (Bernstein et al., 2003). Two trauma-related conditions that share a high prevalence of TCE are post-traumatic stress disorder (PTSD) and borderline personality disorder (BPD). PTSD and BPD share overlapping symptoms (e.g., emotion dysregulation, interpersonal dysfunction) and show disorder-specific profiles (e.g., sleep disturbances) (Hailes et al., 2019; Jowett et al., 2020; Krause-Utz, 2021). TCE might therefore operate as a distal risk factor for PTSD and BPD and might contribute to both shared symptoms and disorder-specific patterns by influencing more proximal mechanisms (Nolen-Hoeksema & Watkins, 2011). Research exploring the impact of TCE on shared biopsychosocial mechanisms in PTSD and BPD is scarce yet essential for advancing prevention and intervention strategies that address overarching TCE-related impairments. Therefore, in this thesis, the links between TCE and three possible mechanisms, namely, disturbances in social functioning, emotion processing, and sleep, were investigated in individuals with PTSD, BPD, as well as healthy controls in three complementary studies. Study 1 investigated the transdiagnostic relationship between TCE and social functioning, and the mechanisms underlying this link, across adults with and without psychopathology through a systematic literature review. TCE were associated with various impairments in social functioning, with mostly small to moderate effect sizes. The most robust links emerged with intimate partner violence (IPV), aggression, social connectedness, attachment, and early maladaptive schemas. Evidence for associations with sexuality, intimate partner relationships, and social-cognitive processes was less consistent. Moreover, the review identified psychopathology (including PTSD and BPD features), insecure attachment, early maladaptive schemas and emotion dysregulation as key mechanisms between TCE and social dysfunction. This motivated the subsequent examination of emotional processes as a further mechanism. Study 2 examined the link between TCE and emotional reactivity and regulation cross-sectionally in women with PTSD, BPD, and healthy controls (HC). A multimethod experimental design was used that integrated self-report, behavioral, and neurophysiological measures (event-related potentials, ERPs). Across participants, higher TCE were correlated with emotional hypo-reactivity to positive (r = -.35, p < .001) and neutral (r = -.22, p = .011) stimuli, consistent with findings of emotional numbing after chronic trauma (Clarke et al., 2024; Sill et al., 2020; Wu et al., 2023). However, this association disappeared once group differences (PTSD, BPD, HC) and medication use were controlled for. Moreover, TCE were not correlated with neurophysiological variables of emotion processing or the effects of instructed emotion regulation (i.e., cognitive reappraisal). In contrast, TCE remained associated with self-reported emotion dysregulation (β = .24, p = .004) even after adjusting for group and medication use. These findings suggest that TCE might confer a more trait-like vulnerability to emotion dysregulation expressed across both disorders but might not strongly shape state-level reactivity to stimuli or the effectiveness of an instructed regulation strategy. Both overlapping and disorder-specific alterations emerged as individuals with PTSD showed greater emotional hypo-reactivity, whereas adults with BPD exhibited heightened global dysregulation and impulsivity. Study 3 explored the association between TCE and past-month and past-night sleep disturbances across three complementary samples. These included treatment-seeking PTSD outpatients and two case-control samples of individuals with PTSD, BPD, and healthy controls. TCE were correlated with poor sleep quality, (nightmare distress), fear of sleep, reduced restorative sleep, pre-sleep psychological balance, increased exhaustion, and psychosomatic symptoms at bedtime (r = .26 to .56, p < .05). However, when emotion dysregulation was taken into account, the direct effect of TCE on sleep became non-significant. These findings might suggest that TCE may serve as a distal risk factor, influencing sleep indirectly through more proximal affective mechanisms. Emotion dysregulation was associated with poorer past-month sleep quality, (nightmare distress), fear of sleep and past-night sleep disturbances above and beyond hyperarousal, group and TCE (β = .21 to .37; p < .046). Individuals with PTSD and BPD overlapped on sleep disturbances. However, fear of sleep remained specifically elevated in PTSD, while emotion dysregulation appeared to largely account for sleep disturbances in BPD. In conclusion, this thesis aimed to address the lack of research on the link between TCE and proximal mechanisms in trauma-related disorders such as PTSD and BPD. Findings across three studies indicated that TCE might act as a broad vulnerability factor, associated with disturbances in social functioning (Study 1), emotional processing (Study 2), and sleep (Study 3). Emotion dysregulation emerged as a central mechanism linking TCE to social impairment and sleep disturbance. At the same time, disorder-specific alterations after TCE were evident (e.g. fear of sleep in PTSD; impulsivity in BPD) that were in line with Ehlers & Clark’s (2000) cognitive model of PTSD and Linehan’s (1993) biosocial model of BPD. These patterns support integrating dimensional and categorical perspectives to develop comprehensive models of trauma-related psychopathology. The results support mechanism-focused assessments in clinical practice and suggest that early stabilization of emotion regulation may help to mitigate downstream interpersonal and sleep disturbances. Depending on individual profiles, transdiagnostic treatments may be used next to disorder-specific interventions to target shared mechanisms (Bohus & Vonderlin, 2024; Cloitre et al., 2002). Limited by the cross-sectional design and focus on two disorders, future research should employ longitudinal, multimodal, and ecologically valid assessments and incorporate data-driven approaches (Goerigk et al., 2023; Huang et al., 2025). Moreover, future research should map mechanisms between TCE and psychopathology across multiple disorders. Specifically, features of complex PTSD (cPTSD) and levels of personality functioning might represent higher-order pathways through which TCE confer transdiagnostic vulnerability while shaping disorder-specific outcomes (Ford & Courtois, 2021; Kampling et al., 2022).
| Dokumententyp: | Dissertationen (Dissertation, LMU München) |
|---|---|
| Themengebiete: | 100 Philosophie und Psychologie
100 Philosophie und Psychologie > 150 Psychologie |
| Fakultäten: | Fakultät für Psychologie und Pädagogik |
| Sprache der Hochschulschrift: | Englisch |
| Datum der mündlichen Prüfung: | 6. Februar 2026 |
| 1. Berichterstatter:in: | Bertsch, Katja |
| MD5 Prüfsumme der PDF-Datei: | c4adc53f1a8766e15ec4da9be9ed3a52 |
| Signatur der gedruckten Ausgabe: | 0001/UMC 31865 |
| ID Code: | 36628 |
| Eingestellt am: | 10. Apr. 2026 14:33 |
| Letzte Änderungen: | 15. Apr. 2026 13:22 |