Theories and Mechanisms

At present, there is no fully adequate theory of motion sickness. Sensory conflict theories relate the elicitation of sickness to "conflicts" between what the vestibular system is transducing and what other senses (e.g., vision) are signaling, or between what the canals and otoliths are specifying, about ongoing body orientation or motion. However, these theories lack predictive power and cannot identify why some conflicts are provocative and others not, nor why exposure to certain forms of motion, such as linear oscillation, are provocative primarily for specific frequencies.

Experimental animals show profound decrease in sensitivity to many emetic drugs after bilateral labyrinthectomy. This has led to the view that motion sickness is a "poison response" including two primary components, stomach emptying and a stress response. Most of the autonomic and endocrine changes occurring during motion sickness do accompany stress responses as well. Removal of the vestibular projection areas of the cerebellum (the nodulus and uvula) renders monkeys insusceptible to motion sickness; it is yet to be determined whether such removal also eliminates the vomiting response to emetic drugs.

Emesis is achieved by the coordinated activity of both smooth and somatic muscles to generate appropriate changes in intra-abdominal and intra-thoracic pressures, and opening of the esophageal sphincters. The central nervous system coordinating mechanisms are complex and only recently have become well understood. In severe motion sickness with multiple bouts of vomiting, alkalosis may develop because of hydrogen ion loss and lead to increased renal excretion of potassium bicarbonate resulting in potassium deficiency which can cause muscle weakness, constipation, and cardiac arrhythmias.

Sodium loss can lead to hypotension. Levels of antidiuretic hormone release also become elevated. The presence of a functioning vestibular system is not necessary for vomiting to be produced. Emesis can be evoked by activation of a variety of peripheral and central afferent mechanisms. Earlier notions of a well-defined "vomiting center" in the brainstem have not been supported by neuroanatomical studies which point instead to a more broadly distributed neuronal representation in the medulla oblongata. The input circuitry controlling emesis is plastic, allowing changes in the sensitivity of other pathways when one is interrupted.

Predicting susceptibility to motion sickness is very difficult. Susceptibility in one exposure condition may not generalize to other situations. Although the vestibular system is essential for motion sickness, susceptibility is not related to vestibular sensitivity per se. Motion sickness can be induced, for example, by motions that stimulate separately or in combination the semicircular canals and otolith organs of the inner ear, moving patterns of visual stimuli, or the voluntary override of reflexive eye movements.

Artificial alteration of the effective gain of the vestibuloocular reflex by means of lens systems readily induces symptoms until adaptive compensations are made. Head movements made during passive body rotation produce a bizarre pattern of stimulation of the canals and otolith organs, "Coriolis cross-coupling stimulation," that is highly provocative under ground-based conditions, only mildly provocative under weightless conditions, and extraordinarily provocative under conditions of increased background force level, e.g., high-G conditions. Individuals often vary in their susceptibility to these different forms of stimulation.

Almost all nonlaboratory situations that are provocative involve more than one etiological or predisposing factor. This largely accounts for why it is difficult to generalize from laboratory assessments of susceptibility involving one or a few factors to more complicated, natural exposure situations that can involve both passive and active head and body movements, and voluntary locomotion.

Exposure to orbital space flight affects not only the otolith organs because of the effective lifting of the tonic 1 g acceleration of earth gravity (owing to the free fall conditions) but also the entire pattern of sensory-motor control and support of the body. Such altered sensory-motor demands during head and body movement are provocative in themselves when mimicked under terrestrial conditions. It is not surprising, therefore, that reports of motion sickness are commonplace with the use of virtual reality devices, which can produce alterations in visuomotor control and in the apparent visual consequences of self-motion. Such cybersickness can be as disruptive during exposure to virtual environments as space sickness is in space flight until adaptive compensation can be achieved.

 An important aspect of space motion sickness and of cybersickness is what has become known as the sopite syndrome (from the Greek "sopor," for drowsiness). It refers to the tiredness, mood swings, lack of initiative and apathy that can develop and persist during prolonged exposure to relatively unprovocative situations. Under some conditions, and for some individuals, the sopite syndrome can be the primary or sole expression of motion sickness. Its presence can be difficult to identify in nonlaboratory settings.