Seasickness, Sea Legs, and Gravity: Suppression of Motion Sickness, Development of Sea Legs, The Role of the Striated Organelle in the Vestibular Efferent System.

Background/

Objectives

In a recent article we outlined how the vestibular efferent system connects the stereo/kinociliary complex at the apex of the macular vestibular hair cells of the inner ear and coordinates movement so that planned body movements are precisely timed to coordinate with the expected otoconial movement that the body movement induces.

Methods

Our present article proposes an extension of this concept with details about how a sailor develops "sea legs." The rocking motion of a boat in rough seas requires sailors to sway in order to remain vertical. This causes fluctuation in the gravity-referenced otoconial signal.

Results

As a sailor develops sea legs, it is necessary that the routine vestibular efferent system activity (based on gravity-referenced orientation on land) is disrupted as the otoconia move with this rocking process in order to re-coordinate with the new otoconial movement. As a result, the cerebral cortex must reconfigure vestibular efferent activity so that the stereo/kinociliary complex moves in conjunction with the otoconial movement. This process is carried out via the striated organelle (STO) and is one that takes several days. Those who are unfortunate and have severe motion sickness, become extremely unwell with nausea, vomiting, severe unsteadiness, and anorexia during this time.

Conclusions

The present article describes how "sea legs" develop and discusses why an unpleasant symptom set can accompany it. We will also outline how a new medication, a calcitonin gene-related peptide (CGRP) inhibitor, which is presently used for the treatment of vestibular dysfunction, has been shown to suppress vestibular efferent activity and may be an effective therapy for these overly symptomatic individuals.