Can threatening virtual reality protocols induce acute anxiety sufficient to cause physiological responses consistent with noradrenergic system activation? — The Association Specialists
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  3. Can threatening virtual reality protocols induce acute anxiety sufficient to cause physiological responses consistent with noradrenergic system activation?

Can threatening virtual reality protocols induce acute anxiety sufficient to cause physiological responses consistent with noradrenergic system activation? (21510)

James H O'Loughlin 1 , Christopher Latella 1 , Janet L Taylor 2
  1. Neurophysiology Research Laboratory, School of Medical and Health Sciences, Edith Cowan University, Joondalup, Western Australia, Australia
  2. Neuroscience Research Australia, Randwick, New South Wales, Australia

The noradrenergic system is engaged by many stimuli, including acute anxiety (AA), with widespread influence on autonomic systems. This study aimed to create AA using threatening virtual reality protocols (VRP) and determine whether physiological responses were consistent with noradrenergic system activation.

Naïve participants (n=10), underwent nine 3-min trials comprising six different threat VRP (overt threat [OT], implied threat [IT1-IT5]), two relaxing control VRP, and one mental arithmetic task (MA). Participants reported anxiety scores after each trial (1-5 Likert-scale [1=not anxious at all, 5=extremely anxious]). Pupil diameter (PD), galvanic skin response (GSR) and heart rate (HR) were recorded with means calculated from 0.5-2.5min in each trial. Pressure pain threshold (PPT) was assessed in the last 30s. After repeated measures ANOVAs, post-hoc paired t-tests compared each anxiety-producing protocol to the averaged relaxing protocols (RAVG). Exploratory repeated measures correlations (Rmcorr) were performed between outcome measures across protocols.

Several threat VRP induced mild AA (median=2.5/5) and significant increases in PD (IT5, p<0.001, mean difference [95%CI lower,upper], 12.4% [8.5,16.4]; IT2, p=0.003, 8.1% [4.4,11.9]; OT, p=0.003, 11.4% [6.1,16.8]) and PPT (OT, p=0.014, 119.2mN [43.9,194.4]; IT5, p=0.019, 108.2mN [32.4,183.9]; IT4, p=0.021, 152.3mN [38.6,266]) from RAVG. MA (AA: median=3/5) resulted in significant changes in PD (p=0.016, 10.6% [3.8,17.3]), PPT (p=0.026, 195.9mN [42.7,349]), GSR (p<0.001, -35.7mV [-45.7,-25.7]) from RAVG. Furthermore, PD correlated with PPT (rrm=0.27 [0.029,0.49], p=0.03), PPT with GSR (rrm=-0.3 [-0.5,-0.075], p=0.01), and GSR with HR (rrm=-0.36 [-0.57,-0.17], p=0.00095).

These findings indicate that VRP can successfully create AA, sufficient to cause physiological responses consistent with noradrenergic system activation.