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OC-064 Psychophysiological And Cortical Responses To Visually Induced Motion Sickness
  1. AD Farmer1,
  2. VF Ban2,
  3. V Giampietro3,
  4. P Andrews4,
  5. Q Aziz1
  1. 1Wingate Institute of Neurogastroenterology, Barts and the London, UK
  2. 2Wingate Institute of Neurogastroenterology, Barts and the London, UK
  3. 3Institute of Psychiatry, Kings College London, London, UK
  4. 4Biomedical Sciences, St George’s Hospital Medical School, London, UK

Abstract

Introduction Nausea is an aversive experience, which negatively impacts on quality of life, adherence to treatment and is a cause for discontinuation of the development of novel compounds. Significant knowledge gaps remain in our understanding of the cortical and psychophysiological mechanisms involved in the genesis and maintenance of nausea. We aimed to develop and validate a readily administered a visually induced motion sickness (VIMS) stimulus to examine the psychophysiological changes induced by the stimulus and characterise the changes in cortical activity using functional magnetic resonance imaging (fMRI).

Methods A 10-min video of motion and a control video of a still image were presented to 98 healthy volunteers (mean age 26 years, range 19–58 years, 53 male) in a randomised cross-over design. Validated questionnaires and visual analogue scales (VAS) were used for anxiety and nausea assessment. We monitored validated measures of autonomic and electrogastrographic activity at baseline and continuously thereafter. Subjects were stratified into quartiles based on nausea VAS scores with the upper and lower quartiles considered to be nausea sensitive and resistant respectively. Of these, 28 subjects of the 50 (mean age 25 years, range 20–49 years, 16 males, 11 nausea resistant) were exposed to the motion video during fMRI.

Results All subjects completed the studies without vomiting. The motion video induced nausea in 57/98 subjects (57%) associated with elevation of median nausea VAS scores (2.0 (IRQ 1–3) vs. 1.0 (IRQ 1–1), p = 0.003). Nausea sensitive subjects had lower normogastria:tachygastria (p = 0.048), increased sympathetic (p = 0.002) and decreased parasympathetic tone (p = 0.03) during the motion video in comparison to the control video. The motion video resulted in heightened neuronal activity in the left and right cerebrum, temporal lobe, middle temporal gyrus and occipital lobe (p < 0.004). Compared to nausea resistant subjects, the nausea sensitive group showed a paucity of activity in the left cerebrum, limbic areas and anterior cingulate cortex (p < 0.001).

Conclusion This study provides evidence to validate the motion video as a VIMS stimulus. Additionally, it demonstrates the cortical and psychophysiological changes induced by VIMS. These changes are as a result of the activation of a broad central network, reflecting the multi-dimensional nature of nausea. Sensitivity to VIMS may therefore be as a consequence of failure of, rather than excessive, activation of cortical areas concerned with the interoceptive and affective aspects of nausea.

Disclosure of Interest None Declared.

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