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Despite the widespread use of oral contraceptives (OCs), remarkably little is known about the effects of OCs on emotion, cognition, and behavior. However, coincidental findings suggest that OCs impair the ability to recognize others’ emotional expressions, which may have serious consequences in interpersonal contexts. To further investigate the effects of OCs on emotion recognition, we tested whether women who were using OCs (n = 42) would be less accurate in the recognition of complex emotional expressions than women who were not using OCs (n = 53). In addition, we explored whether these differences in emotion recognition would depend on women’s menstrual cycle phase. We found that women with OC use were indeed less accurate in the recognition of complex expressions than women without OC use, in particular during the processing of expressions that were difficult to recognize. These differences in emotion recognition did not depend on women’s menstrual cycle phase. Our findings, thus, suggest that OCs impair women’s emotion recognition, which should be taken into account when informing women about the side-effects of OC use.
Recent research suggests that the P3b may be closely related to the activation of the locus coeruleus-norepinephrine (LC-NE) system. To further study the potential association, we applied a novel technique, the non-invasive transcutaneous vagus nerve stimulation (tVNS), which is speculated to increase noradrenaline levels. Using a within-subject cross-over design, 20 healthy participants received continuous tVNS and sham stimulation on two consecutive days (stimulation counterbalanced across participants) while performing a visual oddball task. During stimulation, oval non-targets (standard), normal-head (easy) and rotated-head (difficult) targets, as well as novel stimuli (scenes) were presented. As an indirect marker of noradrenergic activation we also collected salivary alpha-amylase (sAA) before and after stimulation. Results showed larger P3b amplitudes for target, relative to standard stimuli, irrespective of stimulation condition. Exploratory post hoc analyses, however, revealed that, in comparison to standard stimuli, easy (but not difficult) targets produced larger P3b (but not P3a) amplitudes during active tVNS, compared to sham stimulation. For sAA levels, although main analyses did not show differential effects of stimulation, direct testing revealed that tVNS (but not sham stimulation) increased sAA levels after stimulation. Additionally, larger differences between tVNS and sham stimulation in P3b magnitudes for easy targets were associated with larger increase in sAA levels after tVNS, but not after sham stimulation. Despite preliminary evidence for a modulatory influence of tVNS on the P3b, which may be partly mediated by activation of the noradrenergic system, additional research in this field is clearly warranted. Future studies need to clarify whether tVNS also facilitates other processes, such as learning and memory, and whether tVNS can be used as therapeutic tool.
Der vorliegende Übersichtsartikel belegt zunächst, warum das Extinktionslernen als ein zentraler Wirkmechanismus der Expositionsbehandlung angesehen wird. Nach Darstellung der lerntheoretischen Grundlagen wird ein Modell präsentiert, das die Grundlagen der Ausformung, Konsolidierung und des Abrufs des Extinktionsgedächtnisses beschreibt. Dieses Gedächtnismodell der Extinktion liefert die Basis für die Diskussion der aktuellen neurowissenschaftlichen Erkenntnisse zum Extinktionslernen. Durch diese Befunde im Tier-, aber auch im Humanbereich ist es gelungen, die neuronalen Schaltkreise der Extinktion relativ gut zu beschreiben. Der Übersichtsartikel gibt eine Zusammenfassung dieser aktuellen Befunde und geht außerdem auf einige Neurotransmittersysteme dieser Schaltkreise ein, zumindest in dem Maße, wie sie für die Befunde zur pharmakologischen Unterstützung des Extinktionslernens relevant sind. Anschließend wird ein integratives Modell vorgestellt, das den Ausgangspunkt für die Optimierung der Extinktion in der Expositionstherapie liefert. Den Abschluss bildet eine Kasuistik, in der diese Optimierungsstrategien nochmals am Beispiel der Behandlung einer Patientin mit Emetophobie für die Praxis verdeutlicht werden.
Abstract
During fear conditioning, a cue (CS) signals an inevitable distal threat (US) and evokes a conditioned response that can be described as attentive immobility (freezing). The organism remains motionless and monitors the source of danger while startle responses are potentiated, indicating a state of defensive hypervigilance. Although in animals vagally mediated fear bradycardia is also reliably observed under such circumstances, results are mixed in human fear conditioning. Using a single‐cue fear conditioning and extinction protocol, we tested cardiac reactivity and startle potentiation indexing low‐level defensive strategies in a fear‐conditioned (n = 40; paired presentations of CS and US) compared with a non‐conditioned control group (n = 40; unpaired presentations of CS and US). Additionally, we assessed shock expectancy ratings on a trial‐by‐trial basis indexing declarative knowledge of the previous contingencies. Half of each group underwent extinction under sham or active transcutaneous vagus nerve stimulation (tVNS), serving as additional proof of concept. We found stronger cardiac deceleration during CS presentation in the fear learning relative to the control group. This learned fear bradycardia was positively correlated with conditioned startle potentiation but not with declarative knowledge of CS‐US contingencies. TVNS abolished differences in heart rate changes between both groups and removed the significant correlation between late cardiac deceleration and startle potentiation in the fear learning group. Results suggest, fear‐conditioned cues evoke attentive immobility in humans, characterized by cardiac deceleration and startle potentiation. Such defensive response pattern is elicited by cues predicting inevitable distal threat and resembles conditioned fear responses observed in rodents.
inhibiting fear-related thoughts and defensive behaviors when they are no longer appropriate to the situation is a prerequisite for flexible and adaptive responding to changing environments. Such inhibition of defensive systems is mediated by ventromedial prefrontal cortex (vmpfc), limbic basolateral amygdala (BLA), and brain stem locus-coeruleus noradrenergic system (Lc-nAs). non-invasive, transcutaneous vagus nerve stimulation (tVnS) has shown to activate this circuit. Using a multiple-day single-cue fear conditioning and extinction paradigm, we investigated long-term effects of tVnS on inhibition of low-level amygdala modulated fear potentiated startle and cognitive risk assessments. We found that administration of tVnS during extinction training facilitated inhibition of fear potentiated startle responses and cognitive risk assessments, resulting in facilitated formation, consolidation and long-term recall of extinction memory, and prevention of the return of fear. these findings might indicate new ways to increase the efficacy of exposure-based treatments of anxiety disorders.
Structural integrity of the insula and emotional facial recognition performance following stroke
(2023)
The role of the human insula in facial emotion recognition is controversially discussed, especially in relation to lesion-location-dependent impairment following stroke. In addition, structural connectivity quantification of important white-matter tracts that link the insula to impairments in facial emotion recognition has not been investigated. In a case–control study, we investigated a group of 29 stroke patients in the chronic stage and 14 healthy age- and gender-matched controls. Lesion location of stroke patients was analysed with voxel-based lesion-symptom mapping. In addition, structural white-matter integrity for tracts between insula regions and their primarily known interconnected brain structures was quantified by tractography-based fractional anisotropy. Our behavioural analyses showed that stroke patients were impaired in the recognition of fearful, angry and happy but not disgusted expressions. Voxel-based lesion mapping revealed that especially lesions centred around the left anterior insula were associated with impaired recognition of emotional facial expressions. The structural integrity of insular white-matter connectivity was decreased for the left hemisphere and impaired recognition accuracy for angry and fearful expressions was associated with specific left-sided insular tracts. Taken together, these findings suggest that a multimodal investigation of structural alterations has the potential to deepen our understanding of emotion recognition impairments after stroke.