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Neural activity during response inhibition associated with improvement of dysphoric symptoms of PTSD after trauma-focused psychotherapy-an EEG-fMRI study.

ABSTRACT: Although trauma-focused cognitive behavioural therapy (TF-CBT) is the frontline treatment for posttraumatic stress disorder (PTSD), up to one half of patients do not respond optimally to this treatment. Inhibitory functions are important for successful management of PTSD, yet there is a dearth of knowledge regarding the extent to which neural mechanisms unpinning response inhibition are associated with TF-CBT response. Treatment-seeking PTSD patients (n = 40) were assessed during a response inhibition task (the Go/No-Go task) while undergoing functional magnetic imaging (fMRI) and event-related potentials (ERP) in separate sessions. PTSD symptom severity was assessed with the Clinician-Administered PTSD Scale, before undergoing nine sessions of TF-CBT. They were then reassessed post-treatment to estimate reduction in fear and dysphoric symptoms of PTSD. Although neural responses during the inhibitory task did not predict overall symptom change, reduced activation in the left precuneus and the right superior parietal cortex predicted greater improvement in dysphoric symptoms. ERP responses during response inhibition indicated that lower P3 peak latency predicted greater reduction of dysphoric symptoms. There were no significant predictors of changes of fear symptoms. These findings indicate that neural activity associated with response inhibition can act as a predictive biomarker of TF-CBT response for PTSD symptoms. This pattern of findings underscores the importance of delineating the role of biomarkers to predict remission of subtypes of PTSD.

SUBMITTER: Bryant RA

PROVIDER: S-EPMC8046805 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Background: Supporting wellbeing beyond symptom reduction is necessary in trauma care. Research suggests increased posttraumatic growth (PTG) may promote wellbeing more effectively than posttraumatic stress disorder (PTSD) symptom reduction alone. Understanding neurobiological mechanisms of PTG would support PTG intervention development. However, most PTG research to-date has been cross-sectional data self-reported through surveys or interviews.Objective: Neural evidence of PTG and its coexistence with resilience and PTSD is limited. To advance neural PTG literature and contribute translational neuroscientific knowledge necessary to develop future objectively measurable neural-based PTG interventions.Method: Alpha frequency EEG and validated psychological inventories measuring PTG, resilience, and PTSD symptoms were collected from 30 trauma-exposed healthy adults amidst the COVID-19 pandemic. EEG data were collected using custom MNE-Python software, and a wireless OpenBCI 16-channel dry electrode EEG headset. Psychological inventory scores were analysed in SPSS Statistics and used to categorise the EEG data. Power spectral density analyses, t-tests and ANOVAs were conducted within EEGLab to identify brain activity differentiating high and low PTG, resilience, and PTSD symptoms.Results: Higher PTG was significantly differentiated from low PTG by higher alpha power in the left centro-temporal brain area around EEG electrode C3. A trend differentiating high PTG from PTSD was also indicated in this same location. Whole-scalp spectral topographies revealed alpha power EEG correlates of PTG, resilience and PTSD symptoms shared limited, but potentially meaningful similarities.Conclusion: This research provides the first comparative neural topographies of PTG, resilience and PTSD symptoms in the known literature. Results provide objective neural evidence supporting existing theory depicting PTG, resilience and PTSD as independent, yet co-occurring constructs. PTG neuromarker alpha C3 significantly delineated high from low PTG and warrants further investigation for potential clinical application. Findings provide foundation for future neural-based interventions and research for enhancing PTG in trauma-exposed individuals.

Project description:Neurobiological markers of future susceptibility to posttraumatic stress disorder (PTSD) may facilitate identification of vulnerable individuals in the early aftermath of trauma. Variability in resting-state networks (RSNs), patterns of intrinsic functional connectivity across the brain, has previously been linked to PTSD, and may thus be informative of PTSD susceptibility. The present data are part of an initial analysis from the AURORA study, a longitudinal, multisite study of adverse neuropsychiatric sequalae. Magnetic resonance imaging (MRI) data from 109 recently (i.e., ~2 weeks) traumatized individuals were collected and PTSD and depression symptoms were assessed at 3 months post trauma. We assessed commonly reported RSNs including the default mode network (DMN), central executive network (CEN), and salience network (SN). We also identified a proposed arousal network (AN) composed of a priori brain regions important for PTSD: the amygdala, hippocampus, mamillary bodies, midbrain, and pons. Primary analyses assessed whether variability in functional connectivity at the 2-week imaging timepoint predicted 3-month PTSD symptom severity. Left dorsolateral prefrontal cortex (DLPFC) to AN connectivity at 2 weeks post trauma was negatively related to 3-month PTSD symptoms. Further, right inferior temporal gyrus (ITG) to DMN connectivity was positively related to 3-month PTSD symptoms. Both DLPFC-AN and ITG-DMN connectivity also predicted depression symptoms at 3 months. Our results suggest that, following trauma exposure, acutely assessed variability in RSN connectivity was associated with PTSD symptom severity approximately two and a half months later. However, these patterns may reflect general susceptibility to posttraumatic dysfunction as the imaging patterns were not linked to specific disorder symptoms, at least in the subacute/early chronic phase. The present data suggest that assessment of RSNs in the early aftermath of trauma may be informative of susceptibility to posttraumatic dysfunction, with future work needed to understand neural markers of long-term (e.g., 12 months post trauma) dysfunction. Furthermore, these findings are consistent with neural models suggesting that decreased top-down cortico-limbic regulation and increased network-mediated fear generalization may contribute to ongoing dysfunction in the aftermath of trauma.

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Neural activity during response inhibition associated with improvement of dysphoric symptoms of PTSD after trauma-focused psychotherapy-an EEG-fMRI study.

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