The study by Gaikwad et al in this issue reports that younger adults with mild chronic motion sensitivity without known vestibular or central nervous system disorders who performed gaze stabilization exercises had larger improvements in postural stability and motion sensitivity than those who performed saccadic exercises. Postural stability was measured with computerized dynamic posturography with immersion virtual reality (CDP-IVR), and motion sensitivity was measured by the motion sensitivity quotient (MSQ). Motion sensitivity is one sequela of vestibular-related disorders commonly treated by neurologic physical therapists in vestibular rehabilitation.

A history of motion sickness may increase symptoms, and extend the length of recovery, in individuals with vestibular disorders1,2 and concussions.3 Motion sensitivity is a key diagnostic criterion of persistent postural perceptual disorder4 and is highly prevalent in individuals with vestibular migraines.5 Therefore, interventions that reduce impairments associated with motion sensitivity should be of interest to neurologic physical therapists. Individualized supervised exercise programs have been the standard for vestibular rehabilitation.1,6 Therapists use a problem-based approach in prescribing interventions where exercises and activities are matched to the specific problems identified in the examination.1,7 Interventions may also target specific neuroplasticity mechanism therapists hope to affect in patients. Therefore, understanding the potential mechanisms should help therapists' clinical reasoning when selecting an intervention. We are interested in how gaze stabilization exercises or saccadic exercises could account for the reduced motion sensitivity and visually provoked postural instability suggested in this study by Gaikwad et al.

Gaze stabilization exercises are fundamental to vestibular rehabilitation. Vestibular adaptation or substitution is the primary mechanism that supports use of gaze stabilization exercise.1 In most cases, a therapist's intention is to affect vestibular adaptation of the vestibular ocular reflex by upregulating vestibular-ocular gains in individuals with reduced vestibular ocular reflex function, for example, when they show impairment on a head impulse test or dynamic visual acuity (DVA). Therapists may prescribe gaze stabilization exercises to decrease head motion sensitivity based on habituation principles. This is especially true in a situation in which a patient is symptomatic during but has a normal acuity on the DVA8 or when he or she cannot tolerate head movement speeds required for vestibular adaptation. The X1 viewing activity requires repetitive head movements, but is usually prescribed at lower velocities or short durations when the intention is habituation. Head movement exercises may have a generalized effect that employs both habituation and adaptation in the vestibular system. A previous study compared gaze stabilization to head and body habituation exercises after acute vestibular hypofunction and found that both interventions, rather than a specific type of exercise, improved DVA and reduced motion sensitivity as measured by the MSQ.9

In the study by Gaikwad et al, despite the change in mean MSQ score reaching statistical significance, therapists should be cautious in inferring that gaze stabilization exercise had meaningful clinical effect on these individuals' head and body motion sensitivity. The MSQ does not have established minimal clinical difference or minimal clinical important difference scores to interpret these changes, and participants had no change in severity category, mild motion sensitivity,6 or motion sensitivity susceptibility. Motion sensitivity quotient scores less than 10 are likely to be influenced by a floor effect.10 Other outcome measures may add more clinical value, such as the DVA or subjective ratings scales during the DVA.8

The gaze stabilization exercises are not considered to specifically challenge an individual to resolve a sensory mismatch problem. Typically, therapists use a habituation approach with visual motion or optokinetic stimulation and balance activities under different sensory conditions to address visually provoked postural instability.1 These interventions are thought to reduce visual dependence, which contributes to postural sway in a sensory conflict environment as presented in the CDP-IVR measurements.11 In the study by Gaikwad et al, participants were instructed to perform exercises against a plain background, and there was no progression to add complex visual environments to create visual field motion. Whether gaze stabilization exercises are more effective than visual motion habituation or balance activities in improving postural control in patients with motion sensitivity is yet to be determined.

Forced use of the vestibular system may not be the only reasons these participants had an improvement in postural stability in CDP-IVR C2. Granting that the saccadic exercise group served as the control group, a learning effect could still have explained some of the improvement, because a "very large" effect size12 was reported for both groups. The CDP-IVR C2 condition was also equally difficult for individuals with and without motion sensitivity when first exposed.13 In a similar study, control subjects who did not participate in gaze stabilization exercises also had large improvements in the CDP-IVR C2 performance.14 Sampling distribution may also have affected the results. Lower preintervention scores on the CDP-IVR C2 may account for the larger mean percent improvements in the experimental group, and mean postintervention scores for both groups were essentially not different.

Both groups performed exercises in standing; therefore, participants were practicing using their postural system with a secondary visual task. Learning due to practicing these dual tasks could have transferred to the improved postural stability in the CDP-IVR. Alternatively, gaze stabilization and saccadic exercises may have trained these individuals to improve visual fixation strategies when confronted with visual motion stimulus. Winkler and Ciuffreda15 showed that individuals with vestibular dysfunction and visual motion sensitivity had increased saccadic corrections in the presence of a visual moving background as compared with healthy individuals or individuals with vestibular disorders without visual motion sensitivity. Both exercises required the participants to repeatedly focus their vision for several minutes a day and may have contributed to better visual fixation strategies that reduced postural sway under moving visual environments.

In summary, while the results of the study by Gaikwad et al are interesting and potentially valuable, clinicians should be cautious in generalizing the results of this study to patient populations with more severe motion sensitivity who are treated with vestibular rehabilitation. The mechanisms underlying the improvement seen in this study require additional investigation. We do not know whether other interventions, habituation programs of movement, or exposure to optokinetic or visual motion would provide better outcomes for patients with motion sensitivity. Future research that compares outcomes of various treatment approaches and better defines criteria for selecting and progressing interventions for individuals with motion sensitivity is needed.

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