GAZE STABILITY DURING CHAIR-RISE: EFFECTS OF VESTIBULOPATHY. Naseem Challawala*1; David Krebs2; Kathleen Gill-Body2; Chris McGibbon3 1. Spaulding Rehabilitation Hospital, Boston, MA; 2. Physical Therapy, MGH-Institute of health professions, Boston, MA; 3. University of New Brunswick, Fredericon, NB, Canada PURPOSE: The purposes of our study were 1. To determine if gaze pitch stability differed between healthy people and individuals with vestibulopathy during chair rise, and 2. To examine the extent to which a timed measure of functional mobility, the Timed Up and Go score (TUG), could be explained by gaze stability during chair-rise. We hypothesized that during chair-rise 1) healthy individuals would have better pitch gaze stability than individuals with vestibulopathy, and that 2) lower gaze stability would predict higher TUG scores in individuals with vestibulopathy. BACKGROUNDS/SIGNIFICANCE: Individuals with vestibular dysfunction often have gaze instability, low head to eye velocity gains, and poor phase timing of eye movement in relation to head movement. These vestibulo-ocular reflex (VOR) impairments engender inaccurate perception of the environment when the body is moving, which may impair posture and balance during day-to-day activities. Although VOR function is reportedly impaired during functional activities including walking, sitting and standing in place in individuals with vestibular dysfunction VOR function during chair-rise has not been studied among patients with vestibulopathy. Because gaze stability has not been reported in elders during chair-rise, we examined a wide range of both healthy and vestibulopathic individuals. Individuals with vestibular dysfunction also often have balance impairments that lead to decreased functional mobility, but whether balance impairments can be explained by their difficulty in maintaining gaze stability is unknown. SUBJECTS: Twenty subjects with vestibulopathy (mean age 56.5 years), 13 with unilateral vestibular hypofunction (UVH) and 7 with bilateral vestibular hypofunction (BVH) were included in this study. The control group consisted of sixteen age matched healthy subjects (mean age 52.74 years,) with no balance or neuromusculoskeletal impairments according to their medical history and physical examination. METHODS AND MATERIALS: A backless, armless chair adjusted to 100% of each subject's knee height was used for all subjects during chair-rise. Eye movement data were collected using an ISCAN video pupil tracking system (Model RK-726 PCI, ISCAN Inc. Burlington, MA). Four Selspot II (Selective Electronics, Partille, Sweden) optoelectric cameras were used to collect three dimensional body segment kinematic data. Phase plane analysis was used to quantify stability of gaze, eye movement and head movement. Phase plane stability is based on the variance (the standard deviation squared) in displacement and velocity; therefore, the lower the phase plane gaze stability value, the more the data cluster together, signifying less deviation from the target upon which subjects were to foveate. TUG was measured by a stopwatch as the time taken to stand up from a chair, walk a distance of 10 feet, turn around, walk back to the chair and sit down. ANALYSES: One-way Analysis of Variance (ANOVA) was used to compute differences in gaze, eye and head phase plane values, and time differences between peak eye and head velocity and chair-rise time between healthy subjects and subjects with vestibulopathy. Pearson correlation coefficients were used to investigate the relationship between TUG scores and gaze stability for subjects with vestibular hypofunction. All statistical tests were conducted at .05 significance level using SPSS for Windows v10.0 (SPSS Inc., Chicago, IL). RESULTS: Gaze pitch phase plane was significantly lower in healthy subjects as compared to subjects with vestibular hypofunction (p=0.03) during the entire chair rise trial. The time difference between eye and head peak velocity differed significantly between groups (p= 0.04). For the healthy group, peak eye velocity occurred 6.9 ms before peak head velocity. For subjects with vestibulopathy, peak eye velocity occurred 30 ms after peak head velocity. When young healthy subjects were compared to old healthy subjects, gaze phase plane differed significantly during chair-rise (p=.02). There were no significant correlations between TUG scores and gaze phase plane values for subjects with vestibular hypofunction (r= -.30, p=0.23). CONCLUSIONS: Vestibular testing usually occurs in small, darkened laboratories, but the relevance of those data to common patient complaints of oscillopsia is unclear. The present data show, for the first time, that subjects with vestibular hypofunction have significantly lower gaze stability during chair-rise than healthy subjects. These results put into an ecologically realistic context data from other authors, who report that subjects with vestibular hypofunction have reduced gaze stability during passive head-on-trunk rotations, walking in place, and posturography compared to healthy control subjects. Individuals with vestibulopathy have greater gaze stability during sitting or standing in place as compared to locomotion, probably because locomotion involves high frequency head rotations, ranging up to 8 Hz with harmonic components up to 20 Hz which may produce considerable gain and phase changes that cause gaze instability. Chair-rise is generally considered a low frequency task, however, we show differences in gaze stability between the groups during such a task. Decreased gaze stability in elders and subjects with vestibular hypofunction may account for falls and postural imbalance in these populations while carrying out day-to-day functional activities, and these data clearly suggest one mechanism responsible for decreased eye-head coordination leading to retinal slip and oscillopsia among subjects with vestibulopathy. FUNDING SOURCE: None KEYWORDS: Vestibulopathy, Gaze Stability, Chair-rise Copyright 2010 by the American Physical Therapy Association. 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