Category: Adult Anxiety
Keywords: Psychophysiology | Information Processing
Presentation Type: Symposium
Objective: Attention bias modification treatment (ABMT) has been shown to reduce anxiety symptoms in randomized controlled trials. It is typically assumed that this clinical improvement is based on a contingency learning process embedded in the attentional task. However, this assumption has been difficult to substantiate, due to limitations of the response-time measures utilized thus far. A clear marker of learning in ABMT would promote a better understanding of treatment efficacy, which is potentially hindered by deficits in statistical learning in some patients. We will present an application of the visual mismatch negativity (vMMN), a neural prediction-error event-related brain potential (ERP), as a neural marker for contingency learning in ABMT in nonanxious participants and in patients with anxiety disorders.
Method: 25 patients with social anxiety disorder (SAD), 23 patients with generalized anxiety disorder (GAD), and 18 nonanxious controls underwent one session of a dot-probe-based ABMT away from threat while their neural responses were continuously recorded. The session was constructed of 400 trials divided into two blocks, each containing 80% standard ABMT trials (target appearing at neutral face location) and 20% deviant trials (targets appear at angry face locations). vMMN was calculated as the difference between the ERP in response standard trials and the ERP in response to deviant trials. It was expected that vMMN will emerge in the second block in participants who learned the contingency between threat location and target location. Based on previous research it was also expected that vMNN will be less frequently observed in anxious relative to nonanxious participants.
Results: Analysis of averaged ERPs revealed vMMN in response to violations of the contingency embedded in ABMT in the second block of the task (p=0.035). In the first block of trials no significant difference was found between standard and deviant trials, suggesting that a learning process is required to elicit a prediction-error response for this contingency. When examined separately, vMMN was clearly observed in the nonanxious group (p=0.026) but not in the SAD or GAD groups. 68% of the nonanxious participants showed vMMN, while in the SAD group and GAD groups vMMN was observed in only 52% and 43%, respectively (p=0.036).
Conclusions: These findings show promise for the use of vMMN as a possible neuromarker for contingency learning in ABMT. Such a tool could allow better understanding of the learning mechanisms at play in anxiety symptom reduction in ABMT. In addition, these finding reveal a possible deficit in contingency learning of the ABMT task for anxious patients, which may influence their ability to benefit from ABMT.
Tel Aviv University
Friday, November 17
10:15 AM – 11:45 AM
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