Amygdala Deactivation as a Neural Correlate of Pain Processing in Patients with Borderline Personality Disorder and Co-Occurrent Posttraumatic Stress Disorder

Department of Psychosomatic Medicine and Psychotherapy, Central Institute of Mental Health, Mannheim, Germany.
Biological psychiatry (Impact Factor: 10.26). 05/2009; 65(9):819-22. DOI: 10.1016/j.biopsych.2008.10.028
Source: PubMed


Previous studies have revealed altered affective pain processing in patients with borderline personality disorder (BPD) as well as in patients with posttraumatic stress disorder (PTSD). Reduced levels of activation in the amygdala might be related to antinociceptive mechanisms pertinent to both disorders. This study aimed at clarifying whether central antinoceptive mechanisms discriminate BPD patients with and without co-occurrent PTSD.
We investigated 29 medication-free female outpatients with BPD, 12 with and 17 without co-occurrent PTSD. Psychophysical characteristics were assessed, and functional magnetic resonance imaging was performed during heat stimulation with stimuli adjusted for equal subjective painfulness.
No difference in pain sensitivity was found between both groups of patients. Amygdala deactivation, however, was more pronounced in BPD patients with co-occurrent PTSD compared with those without PTSD. Amygdala deactivation was independent of BPD symptom severity and dissociation.
Amygdala deactivation seems to differentiate patients who meet criteria for both BPD and PTSD from BPD patients without co-occurrent PTSD. On the basis of these preliminary findings it might be speculated that reduced pain sensitivity or at least the emotional component of it is associated with amygdala deactivation in patients with both disorders, whereas BPD patients without PTSD use different yet unknown antinociceptive mechanisms.

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    • "Given that any emotional response is a complex, multifaceted phenomenon involving not only subjective experience, but also physiological arousal and motoric behavior, the value of accessing other, much more objective streams of physiological data to complement that of real-time self-report of emotional responding warrants attention (Rosenthal et al., 2008). Specific to the aims of the present study, the ambulatory assessment of physiological responding concurrent with subjective affective reports may prove particularly helpful in clarification of the phenomenology of BPD, PTSD, and BPD-PTSD comorbidity, especially given recent evidence of both similarity and divergence in pathophysiology across these diagnostic groups (e.g., Kraus et al., 2009; Limberg et al., 2011; Rodrigues et al., 2011; Schmahl et al., 2004; Schmahl et al., 2009), along with evidence associating subjective arousal with distress in individuals with BPD (Ebner-Priemer et al., 2008). From a treatment perspective , also, the utilization of EMA methods—including advanced physiological measurements—to longitudinally examine affect dysregulation as a marker of treatment outcome may be a critical direction to pursue in the further development and evaluation of treatment protocols designed to address BPD-PTSD comorbidity. "
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    ABSTRACT: Ecological momentary assessment was utilized to examine affective instability (AI) in the daily lives of outpatients with borderline personality disorder (BPD; N = 78), with and without posttraumatic stress disorder (PTSD). A psychiatric control group (n = 50) composed of outpatients with major depressive disorder/dysthymia (MDD/DYS) was employed to compare across subgroups: BPD-only, BPD+PTSD, MDD/DYS-only, and MDD/DYS+PTSD. Compared with the BPD-only group, the BPD+PTSD group had significantly greater instability of fear and sadness, but did not significantly differ in instability of hostility or aggregate negative affect. This pattern of elevated instability of fear and sadness was not present—and, in fact, was reversed—in the MDD/DYS group. Results emphasize the importance of examining AI within the context of specific comorbidities and affect types. Treatment and research addressing AI in the context of BPD-PTSD comorbidity may benefit from a focus on fear and sadness as separate from hostility or general negative affect.
    Full-text · Article · Apr 2015
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    • "With regards to the direction of startle anomalies, our unpublished data (Wiik et al., 2009) and studies of startle in severely traumatized samples, would have predicted blunted startle responses subsequent to neglect and deprivation. There is in fact a growing body of research suggesting that adversity and trauma may cause blunted affect and discordant emotional experiences in a subset of affected individuals (Bremner et al., 1999; Kraus et al., 2009; Rauch et al., 1996). This cluster of anomalies includes restricted range of affect, dissociation, depression, and persistent avoidance symptoms. "
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    Full-text · Article · Mar 2015 · Developmental Psychobiology
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    • "For example, the studies reporting amygdala hyperactivity (e.g., Koenigsberg et al., 2009; Minzenberg et al., 2007; Schulze et al., 2011) involved unmedicated BPD patients, while the studies demonstrating diminished amygdala responsivity included participants currently taking psychotropic medications (Smoski et al., 2011). Similarly, Axis I co-morbidities such as PTSD may influence amygdala reactivity, particularly in relation to pain perception (Kraus et al., 2009). Cullen et al. (2011) reported increased amygdala connectivity during fear states in 12 females with BPD, suggesting increased use of both overt and automatic fear processing; however, the neutral state revealed lower connectivity between both bilateral amygdala and mid-cingulate regions. "
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    Full-text · Article · Oct 2014 · Journal of Psychiatric Research
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