bims-madeba Biomed news
on Mal de débarquement syndrome
Issue of 2019‒02‒03
one paper selected by
Jun Maruta
Mount Sinai Health System

  1. J Neurophysiol. 2019 Jan 30.
    Cohen B, Dai M, Yakushin SB, Cho C.
      Although motion of the head and body has been suspected or known as the provocative cause for generation of motion sickness for centuries, it is only within the last 20 years that the source of the signal generating motion sickness and its neural basis have been firmly established. Here we briefly review the source of the conflicts that cause the body to generate the autonomic signs and symptoms that constitute motion sickness, and provide a summary of the experimental data that has led to an understanding of how motion sickness is generated and can be controlled. Activity and structures that produce motion sickness include vestibular input through the semicircular canals, the otolith organs and the Velocity Storage Integrator in the vestibular nuclei. Velocity Storage is produced through activity of vestibular only (VO) neurons Under control of neural structures in the nodulus of the Vestibulo-Cerebellum. Separate groups of nodular neurons Sens orientation to gravity, roll, tilt and translation and provide strong inhibitory control of the VO neurons. Additionally, there is a strong projection of acetylcholine from the nodulus to the stomach, which along with other serotonergic inputs from the vestibular nuclei could induce nausea and vomiting. Major inhibition is produced by the GABAb agonist, baclofen, that modulates and suppresses activity in the Velocity Storage Integrator. Ingestion of the GABAb agonist baclofen causes suppression of motion sickness. Hopefully, this understanding will lead to better ways to avoid and treat the autonomic signs and symptoms that constitute the syndrome.
    Keywords:  Autonomic System; GABAb agonist; Vestibulo-Only (VO) neurons; baclofen; nodulus