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Cereb Cortex. 2016 Feb;26(2):485-97. doi: 10.1093/cercor/bhu172. Epub 2014 Aug 12.

Brain Circuitry Supporting Multi-Organ Autonomic Outflow in Response to Nausea.

Author information

1
Department of Radiology, Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Charlestown, MA, USA Department of Electronics, Information and Bioengineering, Politecnico di Milano, Milano, Italy Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
2
Department of Radiology, Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Charlestown, MA, USA.
3
Department of Radiology, Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Charlestown, MA, USA Medical School, Universidad de Santander (UDES), Bucaramanga, Colombia.
4
Gastroenterology Unit, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
5
Department of Electronics, Information and Bioengineering, Politecnico di Milano, Milano, Italy.
6
Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
7
Department of Radiology, Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Charlestown, MA, USA Department of Biomedical Engineering, Kyunghee University, Yongin, Korea.

Abstract

While autonomic outflow is an important co-factor of nausea physiology, central control of this outflow is poorly understood. We evaluated sympathetic (skin conductance level) and cardiovagal (high-frequency heart rate variability) modulation, collected synchronously with functional MRI (fMRI) data during nauseogenic visual stimulation aimed to induce vection in susceptible individuals. Autonomic data guided analysis of neuroimaging data, using a stimulus-based (analysis windows set by visual stimulation protocol) and percept-based (windows set by subjects' ratings) approach. Increased sympathetic and decreased parasympathetic modulation was associated with robust and anti-correlated brain activity in response to nausea. Specifically, greater autonomic response was associated with reduced fMRI signal in brain regions such as the insula, suggesting an inhibitory relationship with premotor brainstem nuclei. Interestingly, some sympathetic/parasympathetic specificity was noted. Activity in default mode network and visual motion areas was anti-correlated with parasympathetic outflow at peak nausea. In contrast, lateral prefrontal cortical activity was anti-correlated with sympathetic outflow during recovery, soon after cessation of nauseogenic stimulation. These results suggest divergent central autonomic control for sympathetic and parasympathetic response to nausea. Autonomic outflow and the central autonomic network underlying ANS response to nausea may be an important determinant of overall nausea intensity and, ultimately, a potential therapeutic target.

KEYWORDS:

brain–gut interactions; motion sickness; neuroimaging; parasympathetic; sympathetic

PMID:
25115821
PMCID:
PMC4712791
DOI:
10.1093/cercor/bhu172
[Indexed for MEDLINE]
Free PMC Article

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