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Auton Neurosci. 2017 Jan;202:108-113. doi: 10.1016/j.autneu.2016.10.003. Epub 2016 Oct 17.

Motion sickness increases functional connectivity between visual motion and nausea-associated brain regions.

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Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Harvard Medical School, Boston, MA.
Department of Biomedicine and Prevention, University of Rome Tor Vergata, Rome, Italy.
Korea Institute for Oriental Medicine (KIOM), Daejeon, Korea.
Department of Radiology, Logan University, Chesterfield, MO.
Department of Anesthesiology and Critical Care, Massachusetts General Hospital, Boston, MA.
Department of Biomedical Engineering, Polytechnic Milan, Milan, Italy.
GI Unit, Center for Neurointestinal Health, Massachusetts General Hospital, Boston, MA.
Contributed equally


The brain networks supporting nausea not yet understood. We previously found that while visual stimulation activated primary (V1) and extrastriate visual cortices (MT+/V5, coding for visual motion), increasing nausea was associated with increasing sustained activation in several brain areas, with significant co-activation for anterior insula (aIns) and mid-cingulate (MCC) cortices. Here, we hypothesized that motion sickness also alters functional connectivity between visual motion and previously identified nausea-processing brain regions. Subjects prone to motion sickness and controls completed a motion sickness provocation task during fMRI/ECG acquisition. We studied changes in connectivity between visual processing areas activated by the stimulus (MT+/V5, V1), right aIns and MCC when comparing rest (BASELINE) to peak nausea state (NAUSEA). Compared to BASELINE, NAUSEA reduced connectivity between right and left V1 and increased connectivity between right MT+/V5 and aIns and between left MT+/V5 and MCC. Additionally, the change in MT+/V5 to insula connectivity was significantly associated with a change in sympathovagal balance, assessed by heart rate variability analysis. No state-related connectivity changes were noted for the control group. Increased connectivity between a visual motion processing region and nausea/salience brain regions may reflect increased transfer of visual/vestibular mismatch information to brain regions supporting nausea perception and autonomic processing. We conclude that vection-induced nausea increases connectivity between nausea-processing regions and those activated by the nauseogenic stimulus. This enhanced low-frequency coupling may support continual, slowly evolving nausea perception and shifts toward sympathetic dominance. Disengaging this coupling may be a target for biobehavioral interventions aimed at reducing motion sickness severity.


Brain connectivity; Brain-gut interactions; Heart rate variability; MT+/V5; Sympathovagal balance

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