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PTSD and cognitive symptoms relate to inhibition-related prefrontal activation and functional connectivity.

ABSTRACT: BACKGROUND:Posttraumatic stress disorder (PTSD) is associated with reduced executive functioning and verbal memory performance, as well as abnormal task-specific activity in prefrontal cortex (PFC) and anterior cingulate cortices (ACC). The current study examined how PTSD symptoms and neuropsychological performance in combat veterans relates to (1) medial PFC and ACC activity during cognitive inhibition, and (2) task-independent PFC functional connectivity. METHODS:Thirty-nine male combat veterans with varying levels of PTSD symptoms completed the multisource interference task during functional magnetic resonance imaging. Robust regression analyses were used to assess relationships between percent signal change (PSC: incongruent-congruent) and both PTSD severity and neuropsychological performance. Analyses were conducted voxel-wise and for PSC extracted from medial PFC and ACC regions of interest. Resting-state scans were available for veterans with PTSD. Regions identified via task-based analyses were used as seeds for resting-state connectivity analyses. RESULTS:Worse PTSD severity and neuropsychological performance related to less medial PFC and rostral ACC activity during interference processing, driven partly by increased activation to congruent trials. Worse PTSD severity related to reduced functional connectivity between these regions and bilateral, lateral PFC (Brodmann area 10). Worse neuropsychological performance related to reduced functional connectivity between these regions and the inferior frontal gyrus. CONCLUSIONS:PTSD and associated neuropsychological deficits may result from difficulties regulating medial PFC regions associated with "default mode," or self-referential processing. Further clarification of functional coupling deficits between default mode and executive control networks in PTSD may enhance understanding of neuropsychological and emotional symptoms and provide novel treatment targets.

SUBMITTER: Clausen AN

PROVIDER: S-EPMC5408317 | biostudies-literature | 2017 May

REPOSITORIES: biostudies-literature

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PTSD and cognitive symptoms relate to inhibition-related prefrontal activation and functional connectivity.

Clausen Ashley N AN Francisco Alex J AJ Thelen Joan J Bruce Jared J Martin Laura E LE McDowd Joan J Simmons W Kyle WK Aupperle Robin L RL

Depression and anxiety 20170329 5

<h4>Background</h4>Posttraumatic stress disorder (PTSD) is associated with reduced executive functioning and verbal memory performance, as well as abnormal task-specific activity in prefrontal cortex (PFC) and anterior cingulate cortices (ACC). The current study examined how PTSD symptoms and neuropsychological performance in combat veterans relates to (1) medial PFC and ACC activity during cognitive inhibition, and (2) task-independent PFC functional connectivity.<h4>Methods</h4>Thirty-nine mal ...[more]

PMID: 28370684

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Project description:BackgroundInhibition is a critical executive control process and an established neurobiological phenotype of PTSD, yet to our knowledge, no prospective studies have examined this using a contextual cue task that enables measurement of behavioural response and neural activation patterns across proactive and reactive inhibition.ObjectiveThe current longitudinal study utilised functional magnetic resonance imaging (fMRI) to examine whether deficits in proactive and reactive inhibition predicted PTSD symptoms six months after trauma.MethodTwenty-three (65% males) medical patients receiving emergency medical care from a level 1 trauma centre were enrolled in the study and invited for an MRI scan 1-2-months post-trauma. PTSD symptoms were measured using self-report at scan and 6-months post-trauma. A stop-signal anticipation task (SSAT) during an fMRI scan was used to test whether impaired behavioural proactive and reactive inhibition, and reduced activation in right inferior frontal gyrus (rIFG), ventromedial prefrontal cortex (vmPFC), and bilateral hippocampus, were related to PTSD symptoms. We predicted that lower activation levels of vmPFC and rIFG during reactive inhibition and lower activation of hippocampus and rIFG during proactive inhibition would relate to higher 6-month PTSD symptoms.ResultsNo significant associations were found between behavioural measures and 6-month PTSD. Separate linear regression analyses showed that reduced rIFG activation (F1,21 = 9.97, R2 = .32, p = .005) and reduced vmPFC activation (F1,21 = 5.19, R2 = .20, p = .03) significantly predicted greater 6-month PTSD symptoms; this result held for rIFG activation controlling for demographic variables and baseline PTSD symptoms (β = -.45, p = .04) and Bonferroni correction.ConclusionOur findings suggest that impaired rIFG and, to a lesser extent, vmPFC activation during response inhibition may predict the development of PTSD symptoms following acute trauma exposure. Given the small sample size, future replication studies are needed.HighlightsImpaired inhibition may be an important risk factor for the development of PTSD following trauma, with less right inferior frontal gyrus and ventromedial prefrontal cortex activation during response inhibition predicting PTSD development.

Project description:Depressive disorders contribute heavily to global disease burden; This is possibly because patients are often treated homogeneously, despite having heterogeneous symptoms with differing underlying neural mechanisms. A novel treatment that can directly influence the neural circuit relevant to an individual patient's subset of symptoms might more precisely and thus effectively aid in the alleviation of their specific symptoms. We tested this hypothesis in a proof-of-concept study using fMRI functional connectivity neurofeedback. We targeted connectivity between the left dorsolateral prefrontal cortex/middle frontal gyrus and the left precuneus/posterior cingulate cortex, because this connection has been well-established as relating to a specific subset of depressive symptoms. Specifically, this connectivity has been shown in a data-driven manner to be less anticorrelated in patients with melancholic depression than in healthy controls. Furthermore, a posterior cingulate dominant state-which results in a loss of this anticorrelation-is expected to specifically relate to an increase in rumination symptoms such as brooding. In line with predictions, we found that, with neurofeedback training, the more a participant normalized this connectivity (restored the anticorrelation), the more related (depressive and brooding symptoms), but not unrelated (trait anxiety), symptoms were reduced. Because these results look promising, this paradigm next needs to be examined with a greater sample size and with better controls. Nonetheless, here we provide preliminary evidence for a correlation between the normalization of a neural network and a reduction in related symptoms. Showing their reproducibility, these results were found in two experiments that took place several years apart by different experimenters. Indicative of its potential clinical utility, effects of this treatment remained one-two months later.Clinical trial registration: Both experiments reported here were registered clinical trials (UMIN000015249, jRCTs052180169).

Project description:BACKGROUND:Aberrant activity of the subcallosal cingulate (SCC) is a common theme across pharmacologic treatment efficacy prediction studies. The functioning of the SCC in psychotherapeutic interventions is relatively understudied, as are functional differences among SCC subdivisions. We conducted functional connectivity analyses (rsFC) on resting-state functional magnetic resonance imaging (fMRI) data, collected before and after a course of cognitive behavioral therapy (CBT) in patients with major depressive disorder (MDD), using seeds from three SCC subdivisions. METHODS:Resting-state data were collected from unmedicated patients with current MDD (Hamilton Depression Rating Scale-17 > 16) before and after 14-sessions of CBT monotherapy. Treatment outcome was assessed using the Beck Depression Inventory (BDI). Rostral anterior cingulate (rACC), anterior subcallosal cingulate (aSCC), and Brodmann's area 25 (BA25) masks were used as seeds in connectivity analyses that assessed baseline rsFC and symptom severity, changes in connectivity related to symptom improvement after CBT, and prediction of treatment outcomes using whole-brain baseline connectivity. RESULTS:Pretreatment BDI negatively correlated with pretreatment rACC ~ dorsolateral prefrontal cortex and aSCC ~ lateral prefrontal cortex rsFC. In a region-of-interest longitudinal analysis, rsFC between these regions increased post-treatment (p < 0.05FDR). In whole-brain analyses, BA25 ~ paracentral lobule and rACC ~ paracentral lobule connectivities decreased post-treatment. Whole-brain baseline rsFC with SCC did not predict clinical improvement. CONCLUSIONS:rsFC features of rACC and aSCC, but not BA25, correlated inversely with baseline depression severity, and increased following CBT. Subdivisions of SCC involved in top-down emotion regulation may be more involved in cognitive interventions, while BA25 may be more informative for interventions targeting bottom-up processing. Results emphasize the importance of subdividing the SCC in connectivity analyses.

Project description:Background: Posttraumatic stress disorder (PTSD) is associated with dysregulated neural, cortisol, and cardiac stress reactivity and recovery. This understanding is predominantly based on studies in adults applying emotional-cognitive and trauma-related stimuli inducing negative emotions or perceived threat. Despite large numbers of adolescents with PTSD, few studies are available on neurobiological stress reactivity in this population. Moreover, no previous studies investigated neural reactivity to social-evaluative stress. Objective: To investigate functional brain connectivity, cortisol and cardiac reactivity to acute social-evaluative stress, and additional cortisol measures in trauma-exposed adolescents with and without high PTSD symptoms. Method: A speech preparation task to induce acute social-evaluative stress elicited by anticipatory threat, was used in a subsample of the Amsterdam Born Child and their Development (ABCD) birth cohort, consisting of trauma-exposed adolescents with (n = 20) and without (n = 29) high PTSD symptoms. Psychophysiological interaction analyses were performed to assess group differences in functional connectivity of the hippocampus, mPFC and amygdala during social-evaluative stress and recovery, measured by fMRI. Additionally, perceived stress, heart rate and cortisol stress reactivity and recovery, cortisol awakening response and day curve were compared. Results: The stressor evoked significant changes in heart rate and perceived stress, but not cortisol. The PTSD symptom and control groups differed in functional connectivity between the hippocampus and cerebellum, middle and inferior frontal gyrus, and the mPFC and inferior frontal gyrus during social-evaluative stress versus baseline. Mostly, the same patterns were found during recovery versus baseline. We observed no significant group differences in amygdala connectivity, and cortisol and cardiac measures. Conclusions: Our findings suggest threat processing in response to social-evaluative stress is disrupted in adolescents with PTSD symptoms. Our findings are mainly but not entirely in line with findings in adults with PTSD, which denotes the importance to investigate adolescents with PTSD as a separate population.

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PTSD and cognitive symptoms relate to inhibition-related prefrontal activation and functional connectivity.

Publications

PTSD and cognitive symptoms relate to inhibition-related prefrontal activation and functional connectivity.

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