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Physiological and neural synchrony in emotional and neutral stimulus processing: A study protocol
(2023)
Background: As psychotherapy involves at least two individuals, it is essential to include the interaction perspective research. During interaction, synchrony, i.e., the occurrence of simultaneous responses, can be observed at the physiological, neural, and behavioral level. Physiological responses include heart rate and electrodermal activity; neural markers can be measured using electroencephalogram. Emotionally arousing stimuli are allocated more attentional resources (motivated attention), which is reflected in physiological activation and brain potentials. Here we present a protocol for a pilot study implementing a new research methodology, and replication of the motivated attention to emotion effect in in dyads. There is evidence that higher synchrony is associated with more positive (therapeutic) relationships. Thus, the secondary outcome will be the association between physiological and neural synchrony and subjective ratings.
Methods and design: Individuals (18−30 years) will participate in same-sex pairs in two experiments. In the first experiment (triadic interaction), both participants attentively watch unpleasant, neutral and pleasant pictures, and read/listen to standardized scripts (unpleasant, neutral, and pleasant, respectively) for the imagination task. In the second experiment, participants will read out three scripts (unpleasant, neutral, pleasant) to each other, followed by a joint imagination period. Stimuli will be presented in counterbalanced orders. After each picture and imagination, participants rate their subjective arousal and valence. In the beginning and in the end of the procedure, dyads rate their relationship, sympathy, and bonds (Working Alliance Inventory subscale). Heart rate, electrodermal activity and electroencephalogram will be continuously measured during both experiments using portable devices (EcgMove4 and EdaMove4, nine-channel B-Alert X-Series mobile-wireless EEG). Synchrony analyses will include the dual electroencephalography analysis pipeline, correlational analyses and Actor–Partner Interdependence Models.
Discussion: The present study protocol provides an experimental approach to investigate interpersonal synchrony during emotion processing, allowing for the establishment of research methods in a pilot study, which can later be translated into real-life psychotherapy research. In the future, fundamental understanding of such mechanisms in dyadic interactions is essential in order to promote therapeutic relationships, and thus, treatment effectiveness and efficiency.
Individual responses to behavioral treatment of anxiety disorders vary considerably, which requires a better understanding of underlying processes. In this study, we examined the violation and change of threat beliefs during exposure. From 8,484 standardized exposure records of 605 patients with different anxiety disorders, learning indicators were derived: expectancy violation as mismatch between threat expectancy before exposure and threat occurrence, expectancy change as difference between original and adjusted expectancy after exposure, and prediction-error learning rate as extent to which expectancy violation transferred into change. Throughout sessions, high threat expectancy but low occurrence and adjusted expectancy indicated successful violation and change of threat beliefs by exposure. Expectancy violation, change, and learning rate substantially varied between patients. Not expectancy violation itself, but higher learning rate and expectancy change predicted better treatment outcome. Successful exposure thus requires expectancy violation to induce actual expectancy change, supporting learning from prediction error as transdiagnostic mechanism underlying successful exposure therapy.
Abstract
Background
The need to optimize exposure treatments for anxiety disorders may be addressed by temporally intensified exposure sessions. Effects on symptom reduction and public health benefits should be examined across different anxiety disorders with comorbid conditions.
Methods
This multicenter randomized controlled trial compared two variants of prediction error‐based exposure therapy (PeEx) in various anxiety disorders (both 12 sessions + 2 booster sessions, 100 min/session): temporally intensified exposure (PeEx‐I) with exposure sessions condensed to 2 weeks (n = 358) and standard nonintensified exposure (PeEx‐S) with weekly exposure sessions (n = 368). Primary outcomes were anxiety symptoms (pre, post, and 6‐months follow‐up). Secondary outcomes were global severity (across sessions), quality of life, disability days, and comorbid depression.
Results
Both treatments resulted in substantial improvements at post (PeEx‐I: dwithin = 1.50, PeEx‐S: dwithin = 1.78) and follow‐up (PeEx‐I: dwithin = 2.34; PeEx‐S: dwithin = 2.03). Both groups showed formally equivalent symptom reduction at post and follow‐up. However, time until response during treatment was 32% shorter in PeEx‐I (median = 68 days) than PeEx‐S (108 days; TRPeEx‐I = 0.68). Interestingly, drop‐out rates were lower during intensified exposure. PeEx‐I was also superior in reducing disability days and improving quality of life at follow‐up without increasing relapse.
Conclusions
Both treatment variants focusing on the transdiagnostic exposure‐based violation of threat beliefs were effective in reducing symptom severity and disability in severe anxiety disorders. Temporally intensified exposure resulted in faster treatment response with substantial public health benefits and lower drop‐out during the exposure phase, without higher relapse. Clinicians can expect better or at least comparable outcomes when delivering exposure in a temporally intensified manner.
Extinction learning is suggested to be a central mechanism during exposure-based cognitive behavioralpsychotherapy. A positive association between the patients’pretreatment extinction learning performance andtreatment outcome would corroborate the hypothesis. Indeed, there isfirst correlational evidence between reducedextinction learning and therapy efficacy. However, the results of these association studies may be hampered byextinction-training protocols that do not match treatment procedures. Therefore, we developed an extinction-trainingprotocol highly tailored to the procedure of exposure therapy and tested it in two samples of 46 subjects in total. Byusing instructed fear acquisition training, including a consolidation period overnight, we wanted to ensure that theconditioned fear response was well established prior to extinction training, which is the case in patients with anxietydisorders prior to treatment. Moreover, the extinction learning process was analyzed on multiple response levels,comprising unconditioned stimulus (US) expectancy ratings, autonomic responses, defensive brain stem reflexes, andneural activation using functional magnetic resonance imaging. Using this protocol, we found robust fearconditioning and slow-speed extinction learning. We also observed within-group heterogeneity in extinction learning,albeit a stable fear response at the beginning of the extinction training. Finally, we found discordance betweendifferent response systems, suggesting that multiple processes are involved in extinction learning. The paradigmpresented here might help to ameliorate the association between extinction learning performance assessed in thelaboratory and therapy outcomes and thus facilitate translational science in anxiety disorders
Background: Controversy surrounds the questions whether co-occurring depression has negative effects on cognitivebehavioral therapy (CBT) outcomes in patients with panic disorder (PD) and agoraphobia (AG) and whether treatment for PD and AG (PD/AG) also reduces depressive symptomatology. Methods: Post-hoc analyses of randomized clinical trial data of 369 outpatients with primary PD/AG (DSM-IV-TR criteria) treated with a 12-session manualized CBT (n = 301) and a waitlist control group (n = 68). Patients with comorbid depression (DSM-IV-TR major depression, dysthymia, or both: 43.2% CBT, 42.7% controls) were compared to patients without depression regarding anxiety and depression outcomes (Clinical Global Impression Scale [CGI], Hamilton Anxiety Rating Scale [HAM-A], number of panic attacks, Mobility Inventory [MI], Panic and Agoraphobia Scale, Beck Depression Inventory) at post-treatment and follow-up (categorical). Further, the role of severity of depressive symptoms on anxiety/depression outcome measures was examined (dimensional). Results: Comorbid depression did not have a significant overall effect on anxiety outcomes at post-treatment and follow-up, except for slightly diminished post-treatment effect sizes for clinician-rated CGI (p = 0.03) and HAM-A (p = 0.008) when adjusting for baseline anxiety severity. In the dimensional model, higher baseline depression scores were associated with lower effect sizes at post-treatment (except for MI), but not at follow-up (except for HAM-A). Depressive symptoms improved irrespective of the presence of depression. Conclusions: Exposure-based CBT for primary PD/AG effectively reduces anxiety and depressive symptoms, irrespective of comorbid depression or depressive symptomatology.
The learning theory of panic disorder differs between panic attacks and anxious apprehension as distinct emotional states. Acute panic is accompanied by extreme fear, experience of strong body symptoms reflecting autonomic surge and flight tendencies. In contrast, anxious apprehension is associated with hypervigilance towards bodily sensations and increased distress when subtle somatic symptoms are identified. Following animal models, these clinical entities reflect different stages of defensive reactivity depending upon the imminence of interoceptive or exteroceptive threat cues with lowest distance to threat during panic attacks. We tested this model by investigating the dynamics of defensive reactivity in a large group of patients suffering from panic disorder and agoraphobia (PD/AG) prior to a multicenter controlled clinical trial. Three hundred forty-five patients participated in a standardized behavioral avoidance test (being entrapped in a small, dark chamber for 10 minutes). Defensive reactivity was assessed measuring avoidance and escape behavior, self reports of anxiety and panic symptoms, autonomic arousal (heart rate and skin conductance), and potentiation of the startle reflex before and during the exposure period of the behavioral avoidance test. While 125 patients showed strong anxious apprehension during the task (as indexed by increased reports of anxiety, elevated physiological arousal, and startle potentiation), 72 patients escaped from the test chamber. Active escape was initiated at the peak of the autonomic surge accompanied by an inhibition of the startle response as predicted by the animal model. These physiological responses were observed during 34 reported panic attacks as well. We found evidence that defensive reactivity in PD/AG patients is dynamically organized ranging from anxious apprehension to panic with increasing proximity of interoceptive threat. Importantly, the patients differed quite substantially according defensive reactivity during the behavioral avoidance test despite all patients received the same principal diagnosis. These differences can be explained in part by differences in the disposition according to two genetic variants previously associated with panic disorder. Patients carrying the risk variant of a polymorphism in the neuropeptide S receptor gene showed an overall increased heart rate during the whole behavioral avoidance test reflecting an enhanced sympathomimetic activation and consequently arousal level. During the entrapment situation in which heart rate further increased over an already elevated baseline level, risk variant carriers were prone to experience more panic symptoms. This is in line with the learning perspective of panic disorder, postulating that internal cues of elevated arousal increase the chance of experiencing another panic attack once they have been associated with aversive responses. Furthermore, the risk variant of a polymorphism in the monoamine oxidase A gene was observed to augment the occurrence of panic attacks and escape behavior preparation. In addition, we find evidence that suggest an enhanced resistance to corrective learning experiences as indicated by a lack of a reduction of avoiding and escaping behavior during repeated test chamber exposures in wait-list control patients carrying the risk gene variant. Both effects may strengthen the learning mechanism hypothesized to be involved in the pathogenesis of panic disorder. Exteroceptive and interoceptive cues previously associated with the initial panic attack might trigger subsequent attacks in risk allele carriers more rapidly while simultaneously the opportunity to dissolve once established associations due to contradictory experiences is limited. Now, differential dispositions regarding defensive reactivity in PD/AG patients has to be linked to mechanisms supposed to be involved in exposure based therapy. First outcome evaluations of the clinical trial indicated that a behavioral therapy variant suggested to be linked with higher fear activation during exposure exercises is more effective than another. Further analyses have to proof whether those patients showing a clear specific fear response during the behavioral avoidance test benefit more than others from exposure based therapy.