Labyrinthine lesions and motion sickness susceptibility

Abstract

The angular vestibulo-ocular reflex (aVOR) has a fast pathway, which mediates compensatory eye movements, and a slow (velocity storage) pathway, which determines its low frequency characteristics and orients eye velocity toward gravity. We have proposed that motion sickness is generated through velocity storage, when its orientation vector, which lies close to the gravitational vertical, is misaligned with eye velocity during head motion. The duration of the misalignment, determined by the dominant time constant of velocity storage, causes the buildup of motion sickness. To test this hypothesis, we studied bilateral labyrinthine-defective subjects with short vestibular time constants but normal aVOR gains for their motion sickness susceptibility. Time constants and gains were taken from rotational responses. Motion sickness was generated by rolling the head while rotating, and susceptibility was assessed by the number of head movements made before reaching intolerable levels of nausea. More head movements signified lower motion sickness susceptibility. Labyrinthine-defective subjects made more head movements on their first exposure to roll while rotating than normals (39.8 ± 7.2 vs 13.7 ± 5.5; P < 0.0001). Normals were tested eight times, which habituated their time constants and reduced their motion sickness susceptibility. Combining data from all subjects, there was a strong inverse relationship between time constants and number of head movements (r = 0.94), but none between motion sickness susceptibility and aVOR gains. This provides further evidence that motion sickness is generated through velocity storage, not the direct pathway, and suggests that motion sickness susceptibility can be reduced by reducing the aVOR time constant.

Vestibular dysfunction in migraine: effects of associated vertigo and motion sickness

“…In a recent study of patients with suspected bilateral vestibulopathy, the patients with low VOR gain and relatively preserved TCs showed a strong inverse relationship between the TCs and susceptibility to motion sickness, but none between angular VOR gains and motion sickness susceptibility [40]. These findings suggest that motion sickness may develop through the velocity storage mechanism rather than the direct pathway, and reduced VOR TCs may decrease the susceptibility to motion sickness [40].…”

“…These findings suggest that motion sickness may develop through the velocity storage mechanism rather than the direct pathway, and reduced VOR TCs may decrease the susceptibility to motion sickness [40].…”

Assessment of otolith function using cervical and ocular vestibular evoked myogenic potentials in individuals with motion sickness

“…In the Indian context, Sharma and Aparna (1997) found slightly higher prevalence of motion sickness among Tibetans and Northeast Indians (28%) than Northwest Indians (26%), with higher overall prevalence among males (27.3%) than females (16.8%). Irrespective of the kind of travel involved, the sign and symptoms of motion sickness include epigastria awareness, pallor, headache, drowsiness, cold sweating, nausea and vomiting (Diamond and Markham 1992a;Sharma and Aparna 1997;Dai, Raphan, and Cohen 2007).…”

Controlling motion sickness and spatial disorientation and enhancing vestibular rehabilitation with a user‐worn see‐through display

“…Brainstem circuits in the vicinity of the vestibular nuclei, behaving as mathematical integrators, are thought to mediate this storage process. There is evidence that motion sickness is generated through this velocity storage and can be reduced by reducing the angular vestibular ocular reflex (aVOR) time constant (27). Others (28) support a multi-factor explanation of motion sickness, involving both sensory conflict and eye movement.…”