Neural mechanisms of acute stress and trait anxiety in adolescents

Corr, Rachel; Pelletier-Baldelli, Andrea; Glier, Sarah; Bizzell, Joshua; Campbell, Alana; Belger, Ayşenil

doi:10.1016/j.nicl.2020.102543

Cited by 37 publications

(26 citation statements)

References 81 publications

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“…Akin to the present findings, using both PET and fMRI Pruessner and colleagues observed profound deactivation of the limbic system (including hippocampus) in healthy individuals during an acute psychosocial stress task, with the degree of hippocampal deactivation correlating with the amount of cortisol released in response to the task [34]. These findings were later replicated [35] and commensurate results were recently found in a large sample of adolescents (n = 101) [66]. Similar patterns have also emerged [70].…”

Section: Discussionsupporting

confidence: 86%

Altered relationship between cortisol response to social stress and mediotemporal function during fear processing in people at clinical high risk for psychosis: a preliminary report

Davies

Appiah‐Kusi

Wilson

et al. 2021

Eur Arch Psychiatry Clin Neurosci

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Evidence suggests that people at Clinical High Risk for Psychosis (CHR) have a blunted cortisol response to stress and altered mediotemporal activation during fear processing, which may be neuroendocrine–neuronal signatures of maladaptive threat responses. However, whether these facets are associated with each other and how this relationship is affected by cannabidiol treatment is unknown. We examined the relationship between cortisol response to social stress and mediotemporal function during fear processing in healthy people and in CHR patients. In exploratory analyses, we investigated whether treatment with cannabidiol in CHR individuals could normalise any putative alterations in cortisol-mediotemporal coupling. 33 CHR patients were randomised to 600 mg cannabidiol or placebo treatment. Healthy controls (n = 19) did not receive any drug. Mediotemporal function was assessed using a fearful face-processing functional magnetic resonance imaging paradigm. Serum cortisol and anxiety were measured immediately following the Trier Social Stress Test. The relationship between cortisol and mediotemporal blood-oxygen-level-dependent haemodynamic response was investigated using linear regression. In healthy controls, there was a significant negative relationship between cortisol and parahippocampal activation (p = 0.023), such that the higher the cortisol levels induced by social stress, the lower the parahippocampal activation (greater deactivation) during fear processing. This relationship differed significantly between the control and placebo groups (p = 0.033), but not between the placebo and cannabidiol groups (p = 0.67). Our preliminary findings suggest that the parahippocampal response to fear processing may be associated with the neuroendocrine (cortisol) response to experimentally induced social stress, and that this relationship may be altered in patients at clinical high risk for psychosis.

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Section: Discussionsupporting

confidence: 86%

Altered relationship between cortisol response to social stress and mediotemporal function during fear processing in people at clinical high risk for psychosis: a preliminary report

Davies

Appiah‐Kusi

Wilson

et al. 2021

Eur Arch Psychiatry Clin Neurosci

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show abstract

“…Notably, neurobiologically-inspired treatments such as TMS target comparable networks to elicit clinically meaningful responses (116) and present-centered psychotherapy has been shown to normalize cortico-limbic processing in stress-related disorders (117). To conclude our predictive model demonstrates that an emphasis on modeling individual differences in psychopathology and network-based reconfiguration within the stress network improves prediction and interpretability (45, 118), dovetailing well with recent insights on effective treatment mechanisms.…”

Section: Discussionsupporting

confidence: 64%

“…Within this network, dysregulation has been consistently reported across mood and anxiety disorders (44), suggesting that brain networks implicated in acute stress reactivity are also affected in disorders showing maladaptive stress responses. Comparably, previous work in healthy participants or adolescents with mental disorders has shown that trait anxiety is associated with altered stress-induced activation in key regions of the stress network (45,46). However, most studies focus on average stress-induced brain responses during the task.…”

Section: Introductionmentioning

confidence: 71%

Spatio-temporal dynamics of stress-induced network reconfigurations reflect negative affectivity

Kühnel

Czisch

Sämann

et al. 2021

Preprint

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Background: Chronic stress is an important risk factor in the etiology of mood and anxiety disorders, but exact pathomechanisms remain to be understood. Mapping individual differences of acute stress-induced neurophysiological changes, especially on the level of neural activation and functional connectivity (FC), could provide important insights in how variation in the individual stress response is linked to disease risk. Methods: Using an established psycho-social stress task flanked by two resting-state scans, we measured subjective, physiological, and brain responses to acute stress and recovery in 217 unmedicated participants with and without mood and anxiety disorders. To estimate block-wise changes in stress-induced brain activation and FC, we used hierarchical mixed-effects models based on denoised timeseries within a predefined stress network. We predicted inter- and intra-individual differences in stress phases (anticipation vs. acute stress vs. recovery) and transdiagnostic dimensions of stress reactivity using elastic net and support vector machines. Results: We identified four subnetworks showing distinct changes in FC over time. Subnetwork trajectories predicted the stress phase (accuracy: 71%, pperm<.001) and increases in pulse rate (R2 =.10, pperm<.001). Critically, individual spatio-temporal trajectories of changes across networks also predicted negative affectivity (ΔR2=.08, pperm=.009), but not the presence or absence of a mood and anxiety disorder. Conclusions: Spatio-temporal dynamics of brain network reconfiguration induced by stress reflect individual differences in the psychopathology dimension negative affectivity. These results support the idea that vulnerability for mood and anxiety disorders can be conceptualized best at the level of network dynamics, which may pave the way for improved prediction of individual risk.

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“…The basal ganglia comprise a group of subcortical nuclei responsible primarily for motor control, as well as other roles such as motor learning, executive functions and behaviors, and emotions. Previous studies have demonstrated aberrant neural activity of the putamen, a region that is essential for terminating contextually inappropriate motor and cognitive processes in patients with anxiety disorders (Corr et al, 2021; Guo et al, 2018). Thus, the decreased sFC between the SFA and putamen may signify the reduced synergistic regulation of approach‐avoidance behaviors, which helps to explain the more ambivalent emotions and behavior among individuals with HTA.…”

Section: Discussionmentioning

confidence: 99%

Anomalous static and dynamic functional connectivity of amygdala subregions in individuals with high trait anxiety

Wang

Lau

et al. 2021

Depression and Anxiety

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Background: Trait anxiety is considered a susceptible factor for stress-related disorders, and is characterized by abnormal brain activity and connectivity in the regions related to emotional processing (e.g., the amygdala). However, only a few studies have examined the static and dynamic changes of functional connectivity in trait anxiety.Method: We compared the resting-state static and dynamic functional connectivity (sFC/dFC) in individuals with high trait anxiety (HTA, n = 257) and low trait anxiety (LTA, n = 264) using bilateral amygdala subregions as the seeds, that is, the centromedial amygdala (CMA), basolateral amygdala (BLA), and superficial amygdala (SFA).Results: The CMA, BLA, and SFA all showed reduced sFC with the executive control network (ECN) and anomalous dFC with the default mode network (DMN) in individuals with HTA. The CMA only showed reduced sFC with the ECN and reduced dFC with the DMN in individuals with HTA. The BLA showed reduced sFC with the salience network (mainly in the anterior and median cingulate), and increased dFC between the BLA and the DMN in individuals with HTA compared to those with LTA. Notably, HTA showed widespread anomalous functional connectivity in the SFA, including the visual network, mainly in the calcarine fissure, limbic system (olfactory cortex), and basal ganglia (putamen). Conclusion:The anomalous sFC and dFC in individuals with HTA may reflect altered mechanisms in prefrontal control, salient stimuli processing, and amygdaloidal responsivity to potential threats, leading to alterations in associative, attentional, interpretative, and regulating processes that sustain a threat-related processing bias in HTA individuals.

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Neural mechanisms of acute stress and trait anxiety in adolescents

Cited by 37 publications

References 81 publications

Altered relationship between cortisol response to social stress and mediotemporal function during fear processing in people at clinical high risk for psychosis: a preliminary report

Altered relationship between cortisol response to social stress and mediotemporal function during fear processing in people at clinical high risk for psychosis: a preliminary report

Spatio-temporal dynamics of stress-induced network reconfigurations reflect negative affectivity

Anomalous static and dynamic functional connectivity of amygdala subregions in individuals with high trait anxiety

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