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1 Department of Kinesiology and Physical Education, McGill University, Montreal, Canada; Neurological Sciences Institute, Oregon Health and Science University, Beaverton, Oregon, United States
2 W.H. Coulter Department of Biomedical Engineering, Emory University and Georgia Institute of Technology, Atlanta, Georgia, United States; Neurological Sciences Institute, Oregon Health and Science University, Beaverton, Oregon, United States
3 College of Science, China Agricultural University, Beijing, China; Neurological Sciences Institute, Oregon Health and Science University, Beaverton, Oregon, United States
4 Department of Physiology, University of Alberta, Edmonton, Canada; Neurological Sciences Institute, Oregon Health and Science University, Beaverton, Oregon, United States
5 Neurological Sciences Institute, Oregon Health and Science University, Beaverton, Oregon, United States
* To whom correspondence should be addressed. E-mail: paul.stapley{at}mcgill.ca.
The purpose of this study was to determine the source of postural instability in labyrinthectomized cats during lateral head turns. Cats were trained to maintain the head in a forward orientation and then perform a rapid, large amplitude head turn to left or right in yaw, while standing freely on a force platform. Head turns were biomechanically complex with the primary movement in the yaw plane accompanied by an ipsilateral ear-down roll and nose-down pitch. Cats used a strategy of pushing off by activating extensors of the contralateral forelimb while using all four limbs to produce a rotational moment of force about the vertical axis. Following bilateral labyrinthectomy, the initial components of the head turn and accompanying postural responses were hypermetric, but otherwise similar to those produced before the lesion. However, near the time of peak yaw velocity, the lesioned cats produced an unexpected burst in extensors of the contralateral limbs which thrust the body to the ipsilateral side, leading to falls. This postural error was in the frontal, or roll plane even though the primary movement was a rotation in the horizontal, or yaw plane. The response error decreased in amplitude with compensation but did not disappear. We conclude that lack of vestibular input results in active destabilization of balance during voluntary head movement. We postulate that the postural imbalance arises from the misperception that the trunk was rolling contralaterally, based on signals from neck proprioceptors in the absence of vestibular inputs.
This article has been cited by other articles:
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  A. Haque, M. Zakir, and J. D. Dickman Recovery of Gaze Stability During Vestibular Regeneration J Neurophysiol, February 1, 2008; 99(2): 853 - 865. [Abstract] [Full Text] [PDF]
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J. M. Macpherson, D. G. Everaert, P. J. Stapley, and L. H. Ting Bilateral Vestibular Loss in Cats Leads to Active Destabilization of Balance During Pitch and Roll Rotations of the Support Surface J Neurophysiol, June 1, 2007; 97(6): 4357 - 4367. [Abstract] [Full Text] [PDF]
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