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| Funder | Engineering and Physical Sciences Research Council |
|---|---|
| Recipient Organization | University of Kent |
| Country | United Kingdom |
| Start Date | Sep 30, 2021 |
| End Date | Sep 29, 2024 |
| Duration | 1,095 days |
| Number of Grantees | 2 |
| Roles | Student; Supervisor |
| Data Source | UKRI Gateway to Research |
| Grant ID | 2619598 |
Motion sickness is a common and complex syndrome that occurs as a physiological response to real or perceived motion. Despite decades of research, why or how motion sickness occurs has not yet been understood well enough. The widely accepted theory is that of sensory conflict. The theory posits that motion sickness is caused by sensory mismatch of
motion signals received and transmitted by the eyes and the vestibular system in the inner ear [1]. An array of symptoms for motion sickness appears when the central nervous system receives conflicting information from the multiple sensory systems: the inner ear, eyes, skin pressure receptors and the muscle and joint sensory receptors. The primary symptoms of
motion sickness are nausea and vomiting. Motion sickness is a serious problem for the people who are prone to the ailment. Unfortunately, this continues to be encountered in all modes of modern transportation. The author believes that this problem is set to be exacerbated in future with the rapidly increasing adoption of autonomous vehicle technology in which passengers reportedly feel
increased sickness when sitting in front but not driving. Moreover, motion sickness is an emerging hazard with the proliferation of digital devices and displays [2-3]. Countermeasures for motion sickness can be classified as either pharmacologic or behavioural. Pharmacologic measures include over-the-counter medications such as those
containing antihistamines, anticholinergics, amphetamines and serotonin. Research has shown that the effectiveness of these medications suggest involvement with related neurotransmitters: histamine, acetylcholine, noradrenalin and serotonin [4]. Some medications such as scopolamine, are available only via prescription. Although most current
measures are effective at preventing motion sickness, they do little more than induce drowsiness. Over-the-counter medications, particularly, have adverse effects that can impair cognitive function and thus represent a safety risk for occupational use [5]. Behavioural measures could comprise habituation, reprocessing or desensitisation
treatment protocols [5]. The aim of my proposed area of PhD research is to reduce motion sickness/nausea by using auricular Vagus Nerve Stimulation (aVNS). There exists another technique other than aVNS that uses reprocessing therapy based on alternating vibrating stimulations in both palms generally known as Eye Movement Desensitisation and Reprocessing (EMDR) that will be
explored due to its novelty. EMDR therapy was originally used in psychological counselling studies and is based on eye movement [6]. Using both of these non-invasive techniques, we hypothesize that differences would be evident between participants who were exposed to aVNS and EMDR and those who were not, respectively.
The Vagus nerve is the 10th cranial nerve that originates in the brainstem of the central nervous system and travels throughout the periphery, targeting every major organ in the thorax and abdomen. Neuromodulation in the form of electrical stimulation of the auricular Vagus nerve has a potential promise for electroceutical therapy. aVNS is a non-invasive
Auricular Vagus Nerve Stimulation and Vibro-motor Reprocessing Therapy for Motion Sickness Reduction PhD Proposal by Emmanuel Molefi brain stimulation technique that has been shown to be efficacious in the reduction of stress [7-8]. Study in [9] has shown aVNS as a safe clinical procedure and could be an effective
treatment for Acute Respiratory Distress Syndrome (ARDS) originated by Covid-19 and similar viruses.
University of Kent
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