Neural correlates of emotional reactivity and regulation associated with treatment response in a randomized clinical trial for posttraumatic stress disorder.
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ABSTRACT:
SUBMITTER: Joshi SA
PROVIDER: S-EPMC8019332 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Posttraumatic stress disorder (PTSD) may develop when mechanisms for making accurate distinctions about threat relevance have gone awry. Generalization across conceptually related objects has been hypothesized based on clinical observation in PTSD, but the neural mechanisms remain unexplored. Recent trauma-exposed military veterans (n = 46) were grouped into PTSD (n = 23) and non-PTSD (n = 23). Participants learned to generalize fear across conceptual categories (animals or tools) of semantically related items that were partially reinforced by shock during functional magnetic resonance imaging. Conditioned fear learning was quantified by shock expectancy and skin conductance response (SCR). Relative to veteran controls, PTSD subjects exhibited a stronger neural response associated with fear generalization to the reinforced object category in the striatum, anterior cingulate cortex, amygdala, occipitotemporal cortex, and insula (Z > 2.3; p < 0.05; whole-brain corrected). Based on SCR, both groups generalized the shock contingency to the reinforced conceptual category, but learning was not significantly different between groups. We found that PTSD was associated with an enhanced neural response in fronto-limbic, midline, and occipitotemporal regions to a learned representation of threat that is based on previously established conceptual knowledge of the relationship between basic-level exemplars within a semantic category. Behaviorally, veterans with PTSD were somewhat slower to differentiate threat and safety categories as compared with trauma-exposed veteran controls owing in part to an initial overgeneralized behavioral response to the safe category. These results have implications for understanding how fear spreads across semantically related concepts in PTSD.
| S-EPMC7297719 | biostudies-literature
Project description:Refugees often report heightened emotional reactivity and emotion regulation difficulties and are at high risk for mental health problems. Given that refugees are repeatedly exposed to traumatic events that may cause changes in the brain, the present study examined neural correlates of emotional reactivity and regulation and their associations with refugee features (e.g., cumulative trauma) and the severity of psychiatric symptoms (e.g., post-traumatic stress disorder [PTSD]) in North Korean (NK) refugees. Forty NK refugees with trauma exposure and varying levels of psychopathology and 41 healthy South Korean (SK) controls without trauma exposure participated in this study. They performed an emotion regulation task during a functional magnetic resonance imaging (fMRI) assessment. Region of interest (ROI), whole brain, and generalized psychophysiological interaction (gPPI) analyses were conducted. NK refugees with trauma exposure and varying levels of psychopathology showed increased activation in response to negative socio-affective pictures in regions involved in affective processing, including the amygdala and hippocampus, relative to healthy SK controls without trauma exposure. They also exhibited greater prefrontal cortex (PFC) activation, amygdala-PFC functional connectivity (FC), and hippocampal-PFC FC during emotion regulation. More severe PTSD symptoms were associated with greater hippocampal response to negative pictures (vs. neutral pictures) in NK refugees. This study provides neuroscientific evidence for neural alterations in association with emotional reactivity and regulation in traumatized refugees. These findings may contribute to a better mechanistic understanding of emotional reactivity and regulation in refugees and suggest potential ways to address the emotional and mental problems of traumatized refugees.
| S-EPMC8417257 | biostudies-literature
Project description:BackgroundYouth with anxiety disorders struggle with managing emotions relative to peers, but the neural basis of this difference has not been examined.MethodsYouth (Mage = 13.6; range = 8-17) with (n = 37) and without (n = 24) anxiety disorders completed a cognitive reappraisal task while undergoing functional magnetic resonance imaging. Emotional reactivity and regulation, functional activation, and beta-series connectivity were compared across groups.ResultsGroups did not differ on emotional reactivity or regulation. However, fronto-limbic activation after viewing aversive imagery with and without regulation, as well as affect ratings without regulation, were higher for anxious youth. Neither group demonstrated age-related changes in regulation, though anxious youth became less reactive with age. Stronger amygdala-ventromedial prefrontal cortex connectivity related to greater anxiety in control youth, but less anxiety in anxious youth.ConclusionAnxious youth regulated when instructed, but regulation ability did not relate to age. Viewing aversive imagery related to heightened fronto-limbic activation even after reappraisal. Emotion dysregulation in youth anxiety disorders may stem from heightened emotionality and potent bottom-up neurobiological responses to aversive stimuli. Findings suggest the importance of treatments focused on both reducing initial emotional reactivity and bolstering regulatory capacity.
| S-EPMC8922214 | biostudies-literature
Project description:Attention impairments are common symptoms of posttraumatic stress disorder (PTSD); however, the nature of these impairments remains elusive. Attention impairment may arise as the result of either excessive response to task-irrelevant stimuli or reduced response to task-relevant information. To test the association between PTSD and response to task-relevant and task-irrelevant stimuli, we used a 3-tone novelty auditory oddball task (AOD). We hypothesized that participants with PTSD relative to trauma controls would have less response during novelty processing in the dorsolateral prefrontal cortex (dlPFC) and the anterior cingulate cortex, as well as less response in the dlPFC and the orbitofrontal cortex during target detection. Thirty-one male veterans completed a 3-tone novelty AOD task during functional magnetic resonance imaging. Compared to trauma controls, the PTSD group had reduced response during novelty processing in ventromedial prefrontal cortex, superior/middle frontal gyrus (dlPFC), supplementary motor area/caudate, and in posterior regions including bilateral posterior cingulate cortex. The current results suggest PTSD is associated with a pattern of reduced response to novel stimuli. A disturbed orienting response in these brain regions could theoretically underlie PTSD attention-related symptoms.
| S-EPMC5962434 | biostudies-other
Project description:BackgroundInvoluntary memories are a hallmark symptom of posttraumatic stress disorder (PTSD), but studies of the neural basis of involuntary memory retrieval in posttraumatic stress disorder (PTSD) are sparse. The study of the neural correlates of involuntary memories of stressful events in PTSD focuses on the voluntary retrieval of memories that are sometimes recalled as intrusive involuntary memories, not on involuntary retrieval while being scanned. Involuntary memory retrieval in controls has been shown to elicit activity in the parahippocampal gyrus, precuneus, inferior parietal cortex, and posterior midline regions. However, it is unknown whether involuntary memories are supported by the same mechanisms in PTSD. Because previous work has shown that both behavioral and neural responsivity is slowed in PTSD, we examined the spatiotemporal dynamics of the neural activity underlying negative and neutral involuntary memory retrieval.MethodsTwenty-one individuals with PTSD and 21 non-PTSD, trauma-exposed controls performed an involuntary memory task, while undergoing a functional magnetic resonance imaging scan. Environmental sounds served as cues for well-associated pictures of negative and neutral scenes. We used a finite impulse response model to analyze temporal differences between groups in neural responses.ResultsCompared with controls, participants with PTSD reported more involuntary memories, which were more emotional and more vivid, but which activated a similar network of regions. However, compared to controls, individuals with PTSD showed delayed neural responsivity in this network and increased vmPFC/ACC activity for negative > neutral stimuli.ConclusionsThe similarity between PTSD and controls in neural substrates underlying involuntary memories suggests that, unlike voluntary memories, involuntary memories elicit similar activity in regions critical for memory retrieval. Further, the delayed neural responsivity for involuntary memories in PTSD suggests that factors affecting cognition in PTSD, like increased fatigue, or avoidance behaviors could do so by delaying activity in regions necessary for cognitive processing. Finally, compared to neutral memories, negative involuntary memories elicit hyperactivity in the vmPFC, whereas the vmPFC is typically shown to be hypoactive in PTSD during voluntary memory retrieval. These patterns suggest that considering both the temporal dynamics of cognitive processes as well as involuntary cognitive processes would improve existing neurobiological models of PTSD.
| S-EPMC6024199 | biostudies-literature
Project description:Previous research has shown that individuals with substance use disorder (SUD) and posttraumatic stress disorder (PTSD) have emotional processing difficulties. However, no studies have specifically investigated the role of emotional processing in those with co-morbid SUD-PTSD. This study investigated whether there are more emotional processing abnormalities among patients with SUD-PTSD, than those with either a single diagnosis of PTSD or SUD. Emotional processing was assessed in three groups [1) SUD (without PTSD); 2) PTSD (without SUD); and 3) co-morbid SUD-PTSD] using the Emotional Processing Scale (EPS-25) and the International Affective Picture System (IAPS). Each of the three groups reported evidence of emotional processing dysfunction relative to the normal population. Within the SUD-PTSD group there was significant evidence that the additional impact of trauma increased emotional processing dysfunction but less evidence to suggest that substance use increased emotional processing dysfunction further. These findings call into question current United Kingdom guidelines for the treatment of co-morbid SUD-PTSD, which recommend that the drug or alcohol problem should be treated first.
| S-EPMC5529498 | biostudies-other
Project description:BackgroundDeficits in emotional processing are conceptualized in prevailing models of anxiety to underpin key symptoms of panic disorder (PD). Neuroimaging studies show evidence of aberrant neural functioning in PD patients during emotional processing, however little is understood about how non-conscious emotional processing impacts neural processes.MethodWe examined activation and functional connectivity differences in brain regions involved in emotional processing between PD and healthy controls (HC) during subliminal and supraliminal presentations of facial emotions. Twenty-two PD and 33 HC participants were shown happy, sad, neutral, fear, anger and disgust facial expressions during functional magnetic resonance imaging using a 3T MRI scanner. We performed voxelwise ROI analyses at FWE-corrected p < 0.05 for main effects of group and group*emotion interactions.ResultsThere was less pregenual anterior cingulate cortex (pgACC) activation to subliminal presentations of happy and sad faces in PD compared to HC participants (group*emotion). In addition, PD patients had less pgACC - right amygdala connectivity than HC participants during sad and fear subliminal processing (group*emotion). PD patients also exhibited lower right cerebellum activity across all supraliminal presentations of facial expressions compared to HC.ConclusionThese findings suggest that there is aberrant neural processing in PD patients during both conscious and preconscious processing of both positive and negative stimuli, suggesting impaired recruitment of implicit regulatory networks during affective processing. It appears that PD patients may experience deficits in key regulatory connections between inhibitory and emotional neural networks at very early stages of processing of negative affective states.
| S-EPMC8650813 | biostudies-literature
Project description:Rapid eye movement (REM) sleep disturbances predict poor clinical outcomes in posttraumatic stress disorder (PTSD) and major depressive disorder (MDD). In MDD, REM sleep is characterized by activation of limbic and paralimbic brain regions compared to wakefulness. The neural correlates of PTSD during REM sleep remain scarcely explored, and comparisons of PTSD and MDD have not been conducted. The present study sought to compare brain activity patterns during wakefulness and REM sleep in 13 adults with PTSD and 12 adults with MDD using [¹⁸F]-fluoro-2-deoxy-D-glucose positron emission tomography (PET). PTSD was associated with greater increase in relative regional cerebral metabolic rate of glucose (rCMRglc) in limbic and paralimbic structures in REM sleep compared to wakefulness. Post-hoc comparisons indicated that MDD was associated with greater limbic and paralimbic rCMRglc during wakefulness but not REM sleep compared to PTSD. Our findings suggest that PTSD is associated with increased REM sleep limbic and paralimbic metabolism, whereas MDD is associated with wake and REM hypermetabolism in these areas. These observations suggest that PTSD and MDD disrupt REM sleep through different neurobiological processes. Optimal sleep treatments between the two disorders may differ: REM-specific therapy may be more effective in PTSD.
| S-EPMC3869237 | biostudies-literature
Project description:OBJECTIVE:Prediabetes and type 2 diabetes (i.e., hyperglycemia) are characterized by insulin resistance. These problems with energy metabolism may exacerbate emotional reactivity to negatively valenced stimuli and related phenomena such as predisposition toward negative affect, as well as cognitive deficits. Higher emotional reactivity is seen with hyperglycemia and insulin resistance. However, it is largely unknown how metabolic dysfunction correlates with related neural, hormonal, and cognitive outcomes. METHODS:Among 331 adults from the Midlife in the United States study, eye-blink response (EBR) we cross sectionally examined to gauge reactivity to negative, positive, or neutrally valenced pictures from international affect picture system stimuli proximal to an acoustic startle probe. Increased EBR to negative stimuli was considered an index of stress reactivity. Frontal alpha asymmetry, a biomarker of negative affect predisposition, was determined using resting electroencephalography. Baseline urinary cortisol output was collected. Cognitive performance was gauged using the Brief Test of Adult Cognition by telephone. Fasting glucose and insulin characterized hyperglycemia or the homeostatic model assessment of insulin resistance. RESULTS:Higher homeostatic model assessment of insulin resistance corresponded to an increased startle response, measured by EBR magnitude, for negative versus positive stimuli (R = 0.218, F(1,457) = 5.48, p = .020, euglycemia: M(SD) = .092(.776), hyperglycemia: M(SD) = .120(.881)). Participants with hyperglycemia versus euglycemia showed greater right frontal alpha asymmetry (F(1,307) = 6.62, p = .011, euglycemia: M(SD) = .018(.167), hyperglycemia: M(SD) = -.029(.160)), and worse Brief Test of Adult Cognition by telephone arithmetic performance (F(1,284) = 4.25, p = .040, euglycemia: M(SD) = 2.390(1.526), hyperglycemia: M(SD) = 1.920(1.462)). Baseline urinary cortisol (log10 ?g/12 hours) was also dysregulated in individuals with hyperglycemia (F(1,324) = 5.09, p = .025, euglycemia: M(SD) = 1.052 ± .332, hyperglycemia: M(SD) = .961 (.362)). CONCLUSIONS:These results suggest that dysmetabolism is associated with increased emotional reactivity, predisposition toward negative affect, and specific cognitive deficits.
| S-EPMC5976543 | biostudies-literature
Project description:ContextSocial anxiety disorder is thought to involve emotional hyperreactivity, cognitive distortions, and ineffective emotion regulation. While the neural bases of emotional reactivity to social stimuli have been described, the neural bases of emotional reactivity and cognitive regulation during social and physical threat, and their relationship to social anxiety symptom severity, have yet to be investigated.ObjectiveTo investigate behavioral and neural correlates of emotional reactivity and cognitive regulation in patients and controls during processing of social and physical threat stimuli.DesignParticipants were trained to implement cognitive-linguistic regulation of emotional reactivity induced by social (harsh facial expressions) and physical (violent scenes) threat while undergoing functional magnetic resonance imaging and providing behavioral ratings of negative emotion experience.SettingAcademic psychology department.ParticipantsFifteen adults with social anxiety disorder and 17 demographically matched healthy controls.Main outcome measuresBlood oxygen level-dependent signal and negative emotion ratings.ResultsBehaviorally, patients reported greater negative emotion than controls during social and physical threat but showed equivalent reduction in negative emotion following cognitive regulation. Neurally, viewing social threat resulted in greater emotion-related neural responses in patients than controls, with social anxiety symptom severity related to activity in a network of emotion- and attention-processing regions in patients only. Viewing physical threat produced no between-group differences. Regulation during social threat resulted in greater cognitive and attention regulation-related brain activation in controls compared with patients. Regulation during physical threat produced greater cognitive control-related response (ie, right dorsolateral prefrontal cortex) in patients compared with controls.ConclusionsCompared with controls, patients demonstrated exaggerated negative emotion reactivity and reduced cognitive regulation-related neural activation, specifically for social threat stimuli. These findings help to elucidate potential neural mechanisms of emotion regulation that might serve as biomarkers for interventions for social anxiety disorder.
| S-EPMC4142809 | biostudies-literature