title: Visually induced nausea causes characteristic changes in cerebral, autonomic and endocrine function in humans.
abstract: An integrated understanding of the physiological mechanisms involved in the genesis of nausea remains lacking. We aimed to describe the psychophysiological changes accompanying visually induced motion sickness, using a motion video, hypothesizing that differences would be evident between subjects who developed nausea in comparison to those who did not. A motion, or a control, stimulus was presented to 98 healthy subjects in a randomized crossover design. Validated questionnaires and a visual analogue scale (VAS) were used for the assessment of anxiety and nausea. Autonomic and electrogastrographic activity were measured at baseline and continuously thereafter. Plasma vasopressin and ghrelin were measured in response to the motion video. Subjects were stratified into quartiles based on VAS nausea scores, with the upper and lower quartiles considered to be nausea sensitive and resistant, respectively. Twenty-eight subjects were exposed to the motion video during functional neuroimaging. During the motion video, nausea-sensitive subjects had lower normogastria/tachygastria ratio and cardiac vagal tone but higher cardiac sympathetic index in comparison to the control video. Furthermore, nausea-sensitive subjects had decreased plasma ghrelin and demonstrated increased activity of the left anterior cingulate cortex. Nausea VAS scores correlated positively with plasma vasopressin and left inferior frontal and middle occipital gyri activity and correlated negatively with plasma ghrelin and brain activity in the right cerebellar tonsil, declive, culmen, lingual gyrus and cuneus. This study demonstrates that the subjective sensation of nausea is associated with objective changes in autonomic, endocrine and brain networks, and thus identifies potential objective biomarkers and targets for therapeutic interventions.
authors.affiliation: Centre for Digestive Diseases, Blizard Institute, Wingate Institute of Neurogastroenterology, Barts and the London School of Medicine & Dentistry, Queen Mary University of London, London, E1 2AJ, UK; University Hospitals of North Midlands, Stoke on Trent, Staffordshire, ST4 6QG, UK.
authors.forename: Adam D
authors.initials: AD
authors.lastname: Farmer
authors.forename: Vin F
authors.initials: VF
authors.lastname: Ban
authors.forename: Steven J
authors.initials: SJ
authors.lastname: Coen
authors.forename: Gareth J
authors.initials: GJ
authors.lastname: Sanger
authors.forename: Gareth J
authors.initials: GJ
authors.lastname: Barker
authors.forename: Michael A
authors.initials: MA
authors.lastname: Gresty
authors.forename: Vincent P
authors.initials: VP
authors.lastname: Giampietro
authors.forename: Steven C
authors.initials: SC
authors.lastname: Williams
authors.forename: Dominic L
authors.initials: DL
authors.lastname: Webb
authors.forename: Per M
authors.initials: PM
authors.lastname: Hellström
authors.forename: Paul L R
authors.initials: PL
authors.lastname: Andrews
authors.forename: Qasim
authors.initials: Q
authors.lastname: Aziz
mesh_terms: D000328:Adult; D001341:Autonomic Nervous System / Q000502:physiology*; D016022:Case-Control Studies; D002540:Cerebral Cortex / Q000502:physiology*; D004703:Endocrine System / Q000502:physiology*; D005260:Female; D054439:Ghrelin / Q000097:blood; D006801:Humans; D008297:Male; D008875:Middle Aged; D009041:Motion Sickness / Q000097:blood / Q000503:physiopathology*; D009325:Nausea / Q000097:blood / Q000503:physiopathology*; D014667:Vasopressins / Q000097:blood
chemical_list: D054439:Ghrelin; D014667:Vasopressins