|
 |
|||||||||||||||||||
|
|||||||||||||||||||
|
|||||||||||||||||||
 |
 |
|
|
Gaze Position Corrective Eye Movements in Normal Subjects and in Patients with Vestibular Deficits
aDepartment of Neurology, The Johns Hopkins University, Baltimore, Maryland, USA 21287-6921 bDepartment of Otolaryngology-Head and Neck Surgery, The Johns Hopkins University, Baltimore, Maryland 21287-6921, USA cDepartment of Neuroscience, The Johns Hopkins University, Baltimore, Maryland 21287-6921, USA dDepartment of Ophthalmology, The Johns Hopkins University, Baltimore, Maryland 21287-6921, USA eDepartment of Biomedical Engineering, The Johns Hopkins University, Baltimore, Maryland 21287-6921, USA
Address for correspondence: David S. Zee, M.D., The Johns Hopkins University, Department of Neurology, Pathology 2-210, 600 N. Wolfe Street, Baltimore, MD 21287-6921. Voice: 410-955-3319; fax: 410-614-1746. dzee{at}dizzy.med.jhu.edu
Eye movements in response to high-acceleration head rotations (thrusts) in the horizontal plane from patients with unilateral (UVD) or bilateral vestibular loss (BVD) were recorded. The rapid, gaze-position corrections (GPCs) that appeared when vestibulo-ocular reflex (VOR) slow phases were undercompensatory were characterized. For comparison, eye movements from normal subjects who were asked to generate saccades in the direction opposite head rotation (in the same direction as slow phases) were recorded. This normal-subject model produced responses with spatial and temporal characteristics similar to those from GPCs in patients as follows: When head rotations were generated actively, compared with passively, gaze-position errors and corresponding GPCs were smaller and occurred earlier. During passively generated head thrusts, GPCs still occurred when head rotations were made in total darkness, though their accuracy decreased as the requirement for maintaining gaze on a specific location in space was relaxed. Time of onset of GPCs was not rigidly tied to head kinematics (peak velocity or peak acceleration). Speeds of GPCs, however, were lower than speeds of similar-sized, head-fixed saccades. Finally, during passive and active head thrusts in patients, sustained, high-frequency (20 to 30 Hz) oscillations that appeared as tiny saccades were occasionally observed, one immediately following the other, resembling a compensatory slow-phase response. Taken together, the results suggest that one strategy for overcoming a VOR deficit is to enlist the saccadic system to produce an oculomotor response that is required to compensate for head rotation. This response may come in the form of high-velocity GPCs or smaller-amplitude oscillations.
Key Words: oculomotor • head movement • phase plane • vestibulo-ocular reflex This article has been cited by other articles:
| |||||||||||||||||||||||||||||
 |
 |
