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Cardinal characteristics of somatoform disorders (SFDs) are worry of illness, and impaired affective processing. We used relative frontal alpha asymmetry (FAA), a method to measure functional lateralization of affective processing, to investigate psychobiological correlates of SFDs. With alpha activity being inversely related to cortical network activity, relative FAA refers to alpha activity on the right frontal lobe minus alpha activity on the left frontal lobe. Less relative left frontal activity, reflected by negative FAA scores, is associated with lower positive and greater negative affectivity, such as observed in depression. Due to its negative affective component (illness anxiety), we expected to find less relative left frontal activity pattern in SFDs, and positive associations with self-reported chronic stress and depression symptoms. We recorded resting-state EEG activity with 64 electrodes, placed in a 10-10 system in 26 patients with a primary SFD, 23 patients with a major depressive disorder and 25 healthy control participants. The groups did not differ in FAA. Nevertheless, across all participants, less relative left frontal activity was associated with chronic stress and depression symptoms. We concluded that FAA may not serve as an indicator of SFDs. As the relationship of FAA and depressive symptoms was fully mediated by chronic stress, future studies have to clarify whether the association between FAA and chronic stress may represent a shared underlying factor for the manifestation of mental health complaints, such as depression.

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Objective: Altered interoception may play a major role in the etiology of medically unexplained symptoms (MUS). It remains unclear, however, if these alterations concern noticing of signals or if they are limited to the interpretation of signals. We investigated whether individuals with MUS differ in interoceptive awareness as assessed with the Multidimensional Assessment of Interoceptive Awareness (MAIA) questionnaire. Methods: Study 1: A total of 486 individuals completed the Screening for Somatoform Disorders (SOMS-2). Thirty-two individuals each of the upper and lower decile of the SOMS distribution (low symptom reporters/LSR, high symptom reporters/HSR) completed the MAIA. Study 2: MAIA scores of individuals diagnosed with somatoform disorder (SFD; n = 26) were compared to individuals with major depressive disorder (MDD; n = 25) and healthy controls (HC; n = 26). Results: HSR had lower scores than LSR on the MAIA scales Not-Distracting and Not-Worrying. The SFD and MDD groups showed lower scores than HC on the MAIA scales Not-Distracting, Self-Regulation, and Trusting. The MDD group scored lower than the other two groups on the scales Body Listening and Attention Regulation. There were no group differences on the scale Noticing. Conclusion: HSR, SFD, and MDD patients do not differ from HC in the awareness of noticing of interoceptive signal processing, whereas cognitive facets of interoception, such as distraction or self-regulation are differentially affected. This highlights the necessity of including specifically targeted interventions, which improve interoceptive awareness, in the prevention and treatment of SFDs.

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While aging and stress are both known to affect cognitive functions, little is known on whether and how age modulates stress effects on executive functions and their neural correlates. The current study investigated the effect of acute stress on response inhibition and error processing and their underlying cortical processes in younger and older healthy men, using EEG. Forty-nine participants (30 young) were stressed with the Trier Social Stress Test (16 young, 9 older) or underwent a friendly control procedure (14 young, 10 older) and subsequently performed a Go/No-Go task with two levels of task difficulty while performance (reaction time, error rate), stimulus-locked (N2, P3) and response-locked (Ne, Pe) ERPs were measured. Previous results on age-related cognitive deficits were replicated, with slower responses and reduced and delayed N2 and P3 components, as well as reduced Ne and Pe components in older participants. Independent of age, acute stress improved response inhibition, reflected in higher accuracy for compatible trials and enhanced inhibition-related components (N2, P3 and N2d, P3d of the difference waves No-Go minus Go), and improved error processing, reflected in enhanced error-related components (Ne, Pe and Ne_d, Pe_d of the difference waves error minus correct trial). Our findings indicate that acute stress leads to a reallocation of cognitive resources, strengthening inhibition and error processing in young and older healthy men to a similar degree. Neural generators of the analyzed ERPs are mainly part of the salience network, which is upregulated immediately after stress. This offers an explanation as to why response inhibition, in contrast to other executive functions, improves after acute stress.

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The current study investigated the influence of acute stress and the resulting cortisol increase on response inhibition and its underlying cortical processes, using EEG. Before and after an acute stressor or a control condition, 39 healthy men performed a go/no-go task while ERPs (N2, P3), reaction times, errors, and salivary cortisol were measured. Acute stress impaired neither accuracy nor reaction times, but differentially affected the neural correlates of response inhibition; namely, stress led to enhanced amplitudes of the N2 difference waves (N2d, no-go minus go), indicating enhanced response inhibition and conflict monitoring. Moreover, participants responding to the stressor with an acute substantial rise in cortisol (high cortisol responders) showed reduced amplitudes of the P3 of the difference waves (P3d, no-go minus go) after the stressor, indicating an impaired evaluation and finalization of the inhibitory process. Our findings indicate that stress leads to a reallocation of cognitive resources to the neural subprocesses of inhibitory control, strengthening premotor response inhibition and the detection of response conflict, while concurrently diminishing the subsequent finalization process within the stream of processing.

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The stress hormone cortisol is assumed to influence cognitive functions. While cortisol-induced alterations of declarative memory in particular are well-investigated, considerably less is known about its influence on executive functions. Moreover, most research has been focused on slow effects, and rapid non-genomic effects have not been studied. The present study sought to investigate the impact of acute cortisol administration as well as basal cortisol levels on cognitive flexibility, a core executive function, within the non-genomic time frame. Thirty-eight healthy male participants were randomly assigned to intravenously receive either cortisol or a placebo before performing a task switching paradigm with happy and angry faces as stimuli. Cortisol levels were measured at six points during the experiment. Additionally, before the experiment, basal cortisol measures for the cortisol awakening response were collected on three consecutive weekdays immediately following awakening and 30, 45, and 60min after. First and foremost, results showed a pronounced impact of acute and basal cortisol on reaction time switch costs, particularly for angry faces. In the placebo group, low basal cortisol was associated with minimal switch costs, whereas high basal cortisol was related to maximal switch costs. In contrast, after cortisol injection, basal cortisol levels showed no impact. These results show that cognitive flexibility-enhancing effects of acute cortisol administration are only seen in men with high basal cortisol levels. This result supports the context dependency of cortisol administration and shows the relevance of taking basal cortisol levels into account.

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