scholarly journals Effects of 25 mg oxazepam on emotional mimicry and empathy for pain: a randomized controlled experiment

2017 ◽  
Vol 4 (3) ◽  
pp. 160607 ◽  
Author(s):  
Gustav Nilsonne ◽  
Sandra Tamm ◽  
Armita Golkar ◽  
Karolina Sörman ◽  
Katarina Howner ◽  
...  

Emotional mimicry and empathy are mechanisms underlying social interaction. Benzodiazepines have been proposed to inhibit empathy and promote antisocial behaviour. First, we aimed to investigate the effects of oxazepam on emotional mimicry and empathy for pain, and second, we aimed to investigate the association of personality traits to emotional mimicry and empathy. Participants ( n =76) were randomized to 25 mg oxazepam or placebo. Emotional mimicry was examined using video clips with emotional expressions. Empathy was investigated by pain stimulating the participant and a confederate. We recorded self-rated experience, activity in major zygomatic and superciliary corrugator muscles, skin conductance, and heart rate. In the mimicry experiment, oxazepam inhibited corrugator activity. In the empathy experiment, oxazepam caused increased self-rated unpleasantness and skin conductance. However, oxazepam specifically inhibited neither emotional mimicry nor empathy for pain. Responses in both experiments were associated with self-rated empathic, psychopathic and alexithymic traits. The present results do not support a specific effect of 25 mg oxazepam on emotional mimicry or empathy.

Author(s):  
Kevin Wise ◽  
Hyo Jung Kim ◽  
Jeesum Kim

A mixed-design experiment was conducted to explore differences between searching and surfing on cognitive and emotional responses to online news. Ninety-two participants read three unpleasant news stories from a website. Half of the participants acquired their stories by searching, meaning they had a previous information need in mind. The other half of the participants acquired their stories by surfing, with no previous information need in mind. Heart rate, skin conductance, and corrugator activation were collected as measures of resource allocation, motivational activation, and unpleasantness, respectively, while participants read each story. Self-report valence and recognition accuracy were also measured. Stories acquired by searching elicited greater heart rate acceleration, skin conductance level, and corrugator activation during reading. These stories were rated as more unpleasant, and their details were recognized more accurately than similar stories that were acquired by surfing. Implications of these results for understanding how people process online media are discussed.


2018 ◽  
Vol 14 (3) ◽  
pp. 621-631
Author(s):  
Sebastián Calderón ◽  
Raúl Rincón ◽  
Andrés Araujo ◽  
Carlos Gantiva

Most studies of emotional responses have used unimodal stimuli (e.g., pictures or sounds) or congruent bimodal stimuli (e.g., video clips with sound), but little is known about the emotional response to incongruent bimodal stimuli. The aim of the present study was to evaluate the effect of congruence between auditory and visual bimodal stimuli on heart rate and self-reported measures of emotional dimension, valence and arousal. Subjects listened to pleasant, neutral, and unpleasant sounds, accompanied by videos with and without content congruence, and heart rate was recorded. Dimensions of valence and arousal of each bimodal stimulus were then self-reported. The results showed that heart rate depends of the valence of the sounds but not of the congruence of the bimodal stimuli. The valence and arousal scores changed depending on the congruence of the bimodal stimuli. These results suggest that the congruence of bimodal stimuli affects the subjective perception of emotion.


2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Daisuke Hasegawa ◽  
Ryota Sato ◽  
Osamu Nishida

Abstract Background The use of ultrashort-acting β1-blockers recently has attracted attention in septic patients with non-compensatory tachycardia. We summarized the metabolic and hemodynamic effects and the clinical evidence of ultrashort-acting β1-blockers. Main body A recent meta-analysis showed that ultrashort-acting β1-blockers reduced the mortality in septic patients with persistent tachycardia. However, its mechanism to improve mortality is not fully understood yet. We often use lactate as a marker of oxygen delivery, but an impaired oxygen use rather than reduced oxygen delivery has been recently proposed as a more reasonable explanation of hyperlactatemia in patients with sepsis, leading to a question of whether β1-blockers affect metabolic systems. While the stimulation of the β2-receptor accelerates glycolysis and lactate production, the role of β1-blocker in lactate production remains unclear and studies investigating the role of β1-blockers in lactate kinetics are warranted. A meta-analysis also reported that ultrashort-acting β1-blockers increased stroke volume index, while it reduced heart rate, resulting in unchanged cardiac index, mean arterial pressure, and norepinephrine requirement at 24 h, leading to an improvement of cardiovascular efficiency. On the other hand, a recent study reported that heart rate reduction using fast esmolol titration in the very early phase of septic shock caused hemodynamic instability, suggesting that ultrashort-acting β1-blockers should be started only after completing initial resuscitation. While many clinicians still do not feel comfortable controlling sinus tachycardia, one randomized controlled trial in which the majority had sinus tachycardia suggested the mortality benefit of ultrashort-acting β1-blockers. Therefore, it still deems to be reasonable to control sinus tachycardia with ultrashort-acting β1-blockers after completing initial resuscitation. Conclusion Accumulating evidence is supporting the use of ultrashort-acting β1-blockers while larger randomized controlled trials to clarify the effect of ultrashort-acting β1-blockers are still warranted.


2021 ◽  
Vol 5 ◽  
pp. 247054702110003
Author(s):  
Megan Chesnut ◽  
Sahar Harati ◽  
Pablo Paredes ◽  
Yasser Khan ◽  
Amir Foudeh ◽  
...  

Depression and anxiety disrupt daily function and their effects can be long-lasting and devastating, yet there are no established physiological indicators that can be used to predict onset, diagnose, or target treatments. In this review, we conceptualize depression and anxiety as maladaptive responses to repetitive stress. We provide an overview of the role of chronic stress in depression and anxiety and a review of current knowledge on objective stress indicators of depression and anxiety. We focused on cortisol, heart rate variability and skin conductance that have been well studied in depression and anxiety and implicated in clinical emotional states. A targeted PubMed search was undertaken prioritizing meta-analyses that have linked depression and anxiety to cortisol, heart rate variability and skin conductance. Consistent findings include reduced heart rate variability across depression and anxiety, reduced tonic and phasic skin conductance in depression, and elevated cortisol at different times of day and across the day in depression. We then provide a brief overview of neural circuit disruptions that characterize particular types of depression and anxiety. We also include an illustrative analysis using predictive models to determine how stress markers contribute to specific subgroups of symptoms and how neural circuits add meaningfully to this prediction. For this, we implemented a tree-based multi-class classification model with physiological markers of heart rate variability as predictors and four symptom subtypes, including normative mood, as target variables. We achieved 40% accuracy on the validation set. We then added the neural circuit measures into our predictor set to identify the combination of neural circuit dysfunctions and physiological markers that accurately predict each symptom subtype. Achieving 54% accuracy suggested a strong relationship between those neural-physiological predictors and the mental states that characterize each subtype. Further work to elucidate the complex relationships between physiological markers, neural circuit dysfunction and resulting symptoms would advance our understanding of the pathophysiological pathways underlying depression and anxiety.


2012 ◽  
Vol 13 (12) ◽  
pp. 1206-1214 ◽  
Author(s):  
Elizabeth J. Richardson ◽  
Timothy J. Ness ◽  
David T. Redden ◽  
Christopher C. Stewart ◽  
J. Scott Richards

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