TY - JOUR
T1 - Off-center yaw rotation: effect of naso-occipital linear acceleration on the nystagmus response of normal human subjects and patients after unilateral vestibular loss
AU - Curthoys, IS
AU - Haslwanter, Thomas
AU - Black, RA
AU - Burgess, AM
AU - Halmagyi, GM
AU - Topple, AN
AU - Todd, MJ
PY - 1998/1
Y1 - 1998/1
N2 - Dual search coils were used to record horizontal, vertical and torsional eye movement components of one eye during nystagmus caused by off-center yaw rotation (yaw centrifugation). Both normal healthy human subjects (n = 7) and patients with only one functioning labyrinth (n = 12) were studied in order to clarify how the concomitant linear acceleration affected the nystagmus response. Each subject was seated with head erect on the arm of a fixed-chair human centrifuge, 1 m away from the center of the rotation, and positioned to be facing along a radius; either towards (facing-in) or away from (facing-out) the center of rotation. Both yaw right and yaw left angular accelerations of 10°s-2 from 0 to 200°/s were studied. During rotation a centripetal linear acceleration (increasing from 0 to 1.24 x g units) was directed along the subject's naso-occipital axis resulting in a shift of the resultant angle of the gravitoinertial acceleration (GIA) of 51°in the subject's pitch plane and an increase in the total GIA magnitude from 1.0 to 1.59 x g. In normal subjects during the angular acceleration off-center there were, in addition to the horizontal eye velocity components, torsional and vertical eye velocities present. The magnitude of these additional components, although small, was larger than observed during similar experiments with on-center angular acceleration and the change in these components is attributed to the additional effect of the linear acceleration stimulation. In the pitch plane the average size of the shift of the axis of eye velocity (AEV) during the acceleration was about 8°for a 51°shift of the GIA (around 16% of the GIA shift) so that the AEV-GIA alignment was inadequate. There was a very marked difference in the size of the AEV shift depending on whether the person was facing-in [AEV shift forward (i.e. non-compensatory) of about 4°] or facing-out [AEV shift forward (i.e. compensatory) of around 12°]. The linear acceleration decreased the time constant of decay of the horizontal component of the post-rotatory nystagmus, from an average of 24.8°/s facing-in to an average of 11.3°/s facing-out. The linear acceleration dumps torsional eye velocity in an manner analogous to, but independent of, the dumping of horizontal eye velocity. Patients with UVD had dramatically reduced torsional eye velocities for both facing-in and facing-out headings, and there was little if any shift of the AEV in UVD patients. The relatively small effects of linear acceleration on human canal-induced nystagmus found here confirms other recent studies in humans in contrast to evidence from monkeys and emphasizes the large and important differences between humans and monkeys in otolith-canal interaction. Our results confirm the vestibular control of the axis of eye velocity of humans is essentially head-referenced whereas in monkeys that control is essentially space-referenced.
AB - Dual search coils were used to record horizontal, vertical and torsional eye movement components of one eye during nystagmus caused by off-center yaw rotation (yaw centrifugation). Both normal healthy human subjects (n = 7) and patients with only one functioning labyrinth (n = 12) were studied in order to clarify how the concomitant linear acceleration affected the nystagmus response. Each subject was seated with head erect on the arm of a fixed-chair human centrifuge, 1 m away from the center of the rotation, and positioned to be facing along a radius; either towards (facing-in) or away from (facing-out) the center of rotation. Both yaw right and yaw left angular accelerations of 10°s-2 from 0 to 200°/s were studied. During rotation a centripetal linear acceleration (increasing from 0 to 1.24 x g units) was directed along the subject's naso-occipital axis resulting in a shift of the resultant angle of the gravitoinertial acceleration (GIA) of 51°in the subject's pitch plane and an increase in the total GIA magnitude from 1.0 to 1.59 x g. In normal subjects during the angular acceleration off-center there were, in addition to the horizontal eye velocity components, torsional and vertical eye velocities present. The magnitude of these additional components, although small, was larger than observed during similar experiments with on-center angular acceleration and the change in these components is attributed to the additional effect of the linear acceleration stimulation. In the pitch plane the average size of the shift of the axis of eye velocity (AEV) during the acceleration was about 8°for a 51°shift of the GIA (around 16% of the GIA shift) so that the AEV-GIA alignment was inadequate. There was a very marked difference in the size of the AEV shift depending on whether the person was facing-in [AEV shift forward (i.e. non-compensatory) of about 4°] or facing-out [AEV shift forward (i.e. compensatory) of around 12°]. The linear acceleration decreased the time constant of decay of the horizontal component of the post-rotatory nystagmus, from an average of 24.8°/s facing-in to an average of 11.3°/s facing-out. The linear acceleration dumps torsional eye velocity in an manner analogous to, but independent of, the dumping of horizontal eye velocity. Patients with UVD had dramatically reduced torsional eye velocities for both facing-in and facing-out headings, and there was little if any shift of the AEV in UVD patients. The relatively small effects of linear acceleration on human canal-induced nystagmus found here confirms other recent studies in humans in contrast to evidence from monkeys and emphasizes the large and important differences between humans and monkeys in otolith-canal interaction. Our results confirm the vestibular control of the axis of eye velocity of humans is essentially head-referenced whereas in monkeys that control is essentially space-referenced.
KW - Labyrinth vestibular
KW - Labyrinthectomy
KW - Linear acceleration
KW - Nystagmus
KW - Otoliths
KW - Utricular macula
KW - Vestibular commissures
KW - Vestibular compensation
KW - Vestibulo-ocular
KW - Vestibulo-ocular response
UR - http://www.scopus.com/inward/record.url?scp=0031727470&partnerID=8YFLogxK
U2 - 10.1007/s002210050587
DO - 10.1007/s002210050587
M3 - Article
SN - 0014-4819
VL - 123
SP - 425
EP - 438
JO - Experimental Brain Research
JF - Experimental Brain Research
IS - 4
ER -