Left parietal involvement in motion sickness susceptibility revealed by multimodal magnetic resonance imaging.

Susceptibility to motion sickness varies greatly across individuals. However, the neural mechanisms underlying this susceptibility remain largely unclear. To address this gap, the current study aimed to identify the neural correlates of motion sickness susceptibility using multimodal MRI. First, we compared resting-state functional connectivity between healthy individuals who were highly susceptible to motion sickness (N = 36) and age/sex-matched controls who showed low susceptibility (N = 36). Seed-based analysis revealed between-group differences in functional connectivity of core vestibular regions in the left posterior Sylvian fissure. A data-driven approach using intrinsic connectivity contrast found greater network centrality of the left intraparietal sulcus in high- rather than in low-susceptible individuals. Moreover, exploratory structural connectivity analysis uncovered an association between motion sickness susceptibility and white matter integrity in the left inferior fronto-occipital fasciculus. Taken together, our data indicate left parietal involvement in motion sickness susceptibility.

Multimodal Imaging of Repetitive Transcranial Magnetic Stimulation Effect on Brain Network: A Combined Electroencephalogram and Functional Magnetic Resonance Imaging Study.

Repetitive transcranial magnetic stimulation (rTMS) has been increasingly used to treat many neurological and neuropsychiatric disorders. However, the clinical response is heterogeneous mainly due to our inability to predict the effect of rTMS on the human brain. Our previous investigation based on functional magnetic resonance imaging (fMRI) suggested that neuroimaging-guided navigation for rTMS could be informed by understanding connectivity patterns that correlate with treatment response. In this study, 20 individuals with a balance disorder called Mal de Debarquement Syndrome completed high-density resting-state electroencephalogram (EEG) and fMRI recordings before and after 5 days of rTMS stimulation over both dorsolateral prefrontal cortices. Based on temporal independent component analysis of source-level EEG data, large-scale electrophysiological resting-state networks were reconstructed and connectivity values in each individual were quantified both before and after treatment. Our results show that high-density, resting-state EEG can reveal connectivity changes in brain networks after rTMS that correlate with symptom changes. The connectivity changes measured by EEG were primarily superficial cortical areas that correlate with previously shown default mode network changes revealed by fMRI. Further, higher baseline EEG connectivity values in the primary visual cortex were predictive of symptom reduction after rTMS. Our findings suggest that multimodal EEG and fMRI measures of brain networks can be biomarkers that correlate with the treatment effect of rTMS. Since EEG is compatible with rTMS, real-time navigation based on an EEG neuroimaging marker may augment rTMS optimization.

Resting State Functional Connectivity Signature of Treatment Effects of Repetitive Transcranial Magnetic Stimulation in Mal de Debarquement Syndrome.

Repetitive transcranial magnetic stimulation (rTMS) has been used in experimental protocols to treat mal de debarquement syndrome (MdDS), a neurological condition that represents a maladaptive brain state resulting from entrainment to external oscillating motion. Medical treatments and biomarkers for MdDS remain limited but neuromodulation with rTMS has shown evidence for therapeutic effects. This study took a neuroimaging approach to examine the neuromodulatory effect of rTMS on MdDS. Twenty individuals with MdDS underwent five daily treatments of rTMS over bilateral dorsolateral prefrontal cortex (DLPFC). Participants received 1 Hz over right DLPFC (1200 pulses) followed by 10 Hz over left DLPFC (2000 pulses). Resting state functional magnetic resonance imaging was acquired before and after treatments to determine functional connectivity changes associated with a positive treatment effect. A single-subject-based analysis protocol was developed to capture the degree of resting state functional connectivity (RSFC) between the rTMS target and the entorhinal cortex (EC), an area previously shown to be hypermetabolic in MdDS. Our results showed that rocking motion perception in subjects was modulated by rTMS over the DLPFC. Improvements in symptoms correlated most strongly with a post-rTMS reduction in functional connectivity between the left EC and the precuneus, right inferior parietal lobule, and the contralateral EC, which are part of the posterior default mode network. Positive response to rTMS correlated with higher baseline RSFC between the DLPFC and the EC. Our findings suggest that baseline prefrontal-limbic functional connectivity may serve as a predictor of treatment response to prefrontal stimulation in MdDS and that RSFC may serve as a dynamic biomarker of symptom status.

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

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.

Nuclear medicine evaluation of motion sickness and medications on gastric emptying time.

Diminished gastric motility and lack of bowel sounds have been observed in astronauts aboard the Space Shuttle (4). In this study subjects were given scopolamine 0.6 mg with d-amphetamine 5 mg with and without neostigmine 15 mg. Neostigmine 15 mg alone was also compared with placebo for effect on gastric emptying time. In an additional test, subjects performed head movements in a rotating chair to an end-point of motion sickness short of vomiting. Ten ounces of isotonic saline containing 1 mCl of Tc 99mDPTA was ingested 2 h after the medications and immediately after rotation. The counts from stomach contents were monitored with a Picker small field of view gamma camera every 30 s for 1 h. Gastric motility was inhibited by scopolamine and amphetamine with 14% residual count at the end of 1 h. When neostigmine was added to this combination the results were in the placebo range. Motion sickness produced a profound inhibition of gastric emptying with a 47% residual count. The results indicate that the gastric stasis encountered in space is due mainly to motion sickness with a minimal contribution from the antimotion sickness drugs.