On labyrinthine function loss, motion sickness immunity, and velocity storage

Introduction

The space race set in motion by the Cold War intensified in the 1960s, with the Soviet Union first paving the path to manned space flight in 1961 (1). In high relevance to astronauts’ mission readiness (2–5), experiments conducted in this decade, contrasting persons with functioning and bilaterally non-functioning labyrinths, solidified the contributions of the vestibular inputs to production of spatial perception and motion sickness during exposure to passive motion or microgravity (6). However, all forms of labyrinthine deactivation are not created equal. For example, patients may undergo total vestibular nerve section as a treatment for vertigo due to eighth nerve neuroma or Ménière’s disease (7, 8); others may for varying causes sustain selective damage within the vestibular end-organs while retaining functioning nerves, as may be the case for candidates of vestibular implants (9, 10). Selective inactivation of otolithic signals may even be induced environmentally under microgravity in space. Examining information processing in the central vestibular mechanism known as velocity storage in various contexts of labyrinthine inactivation may shed further light on health and perceptual anomalies during or following space flight.

Keywords: cerebellar nodulus; mal de débarquement; nystagmus; semicircular canals; space flight; spatial orientation; vestibular habituation; vestibulo-ocular reflex (VOR)