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J Neurophysiol 91: 1763-1781, 2004. First published November 26, 2003; doi:10.1152/jn.00611.2002
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Phase-Plane Analysis of Gaze Stabilization to High Acceleration Head Thrusts: A Continuum Across Normal Subjects and Patients With Loss of Vestibular Function

Grace C. Y. Peng1,6, David S. Zee1,2,3,4 and Lloyd B. Minor2,3,5

1 Department of Neurology, The Johns Hopkins University, Baltimore, Maryland 21287 2 Department of Otolaryngology—Head and Neck Surgery, The Johns Hopkins University, Baltimore, Maryland 21287 3 Department of Neuroscience, The Johns Hopkins University, Baltimore, Maryland 21287 4 Department of Ophthalmology, The Johns Hopkins University, Baltimore, Maryland 21287 5 Department of Biomedical Engineering, The Johns Hopkins University, Baltimore, Maryland 21287 6 Department of Biomedical Engineering, The Catholic University of America, Washington, DC 20064

Submitted 29 July 2002; accepted in final form 4 November 2003

We investigated the vestibulo-ocular reflex (VOR) during high-acceleration, yaw-axis, head rotations in 12 normals and 15 patients with vestibular loss [7 unilateral vestibular deficient (UVD) and 8 bilateral vestibular deficient (BVD)]. We analyzed gaze stabilization within a 200-ms window after head rotation began, using phase planes, which allowed simultaneous analysis of gaze velocity and gaze position. These "gaze planes" revealed critical dynamic information not easily gleaned from traditional gain measurements. We found linear relationships between peak gaze-velocity and peak gaze-position error when normalized to peak head speed and position, respectively. Values fell on a continuum, increasing from normals, to normals tested with very high acceleration (VHA = 10,000–20,000°/s2), to UVD patients during rotations toward the intact side, to UVD patients during rotations toward the lesioned side, to BVD patients. We classified compensatory gaze corrections as gaze-position corrections (GPCs) or gaze-velocity error corrections (GVCs). We defined patients as better-compensated when the value of their end gaze position was low relative to peak gaze position. In the gaze plane this criterion corresponded to relatively stereotyped patterns over many rotations, and appearance of high velocity (100–400°/s) GPCs in the gaze plane ending quadrant (150–200 ms after head movement onset). In less-compensated patients, and normals at VHA, more GVCs were generated, and GPCs were generated only after gaze-velocity error was minimized. These findings suggest that challenges to compensatory vestibular function can be from vestibular deficiency or novel stimuli not previously experienced. Similar patterns of challenge and compensation were observed in both patients with vestibular loss and normal subjects.


Address for reprint requests and other correspondence: D. S. Zee, The Johns Hopkins University, Department of Neurology, Pathology 2-210, 600 N. Wolfe St., Baltimore, MD 21287-6921 (E-mail: dzee{at}dizzy.med.jhu.edu).




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