Phase-Plane Analysis of Gaze Stabilization to High Acceleration Head Thrusts: A Continuum Across Normal Subjects and Patients With Loss of Vestibular Function

2004 ◽  
Vol 91 (4) ◽  
pp. 1763-1781 ◽  
Author(s):  
Grace C. Y. Peng ◽  
David S. Zee ◽  
Lloyd B. Minor

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.

1999 ◽  
Vol 9 (6) ◽  
pp. 401-412
Author(s):  
Y.P. Ivanenko ◽  
I. Viaud-Delmon ◽  
A. Sémont ◽  
V.S. Gurfinkel ◽  
A. Berthoz

The aim of this study was to examine whether the chronic loss of vestibular function modifies perceptual and oculomotor responses during torso rotations in darkness. Subjects (4 patients with complete vestibular loss and 7 healthy volunteers) were seated on a rotating chair. Stimuli consisted of sinusoidal chair rotations ( ± 30 ∘ , 0.1 Hz and 0.011 Hz). We used 2 conditions: space stationary head (neck stimulation) and space stationary head and shoulders (torso stimulation). Horizontal eye deviations and slow component of eye movements were analysed. The results showed that eye movements and perception of head motion in space during neck stimulation were similar to those during torso stimulation both in normal and labyrinthine-defective (LD) subjects. During low-frequency chair rotations (0.011 Hz) all subjects perceived illusory head or head and shoulder rotation in space (as if the lower part of the body was stationary relative to the room) and shifted their gaze in the direction of illusory head rotation. In these conditions there was no significant difference in eye movements between normal and LD subjects. During higher frequency chair rotations (0.1 Hz), LD subjects had significantly larger eye deviations as well as increases in the gain of the slow component of eye movements relative to normals. In these conditions patients mostly perceived illusory head or head and shoulder rotation in space while normal subjects mainly perceived the head as stationary in space. The results indicate that 1) neck and torso rotations can evoke similar ocular responses in LD subjects, 2) the chronic loss of vestibular function modifies the representation of axial body segment motion relative to space.


2019 ◽  
Vol 126 (6) ◽  
pp. 1619-1629 ◽  
Author(s):  
Sally M. Rosengren ◽  
Konrad P. Weber ◽  
Sendhil Govender ◽  
Miriam S. Welgampola ◽  
Danielle L. Dennis ◽  
...  

The short-latency vestibulo-collic reflex in humans is well defined for only the sternocleidomastoid (SCM) neck muscle. However, other neck muscles also receive input from the balance organs and participate in neck stabilization. We therefore investigated the sound-evoked vestibular projection to the splenius capitis (SC) muscles by comparing surface and single motor unit responses in the SC and SCM muscles in 10 normal volunteers. We also recorded surface responses in patients with unilateral vestibular loss but preserved hearing and hearing loss but preserved vestibular function. The single motor unit responses were predominantly inhibitory, and the strongest responses were recorded in the contralateral SC and ipsilateral SCM. In both cases there was a significant decrease or gap in single motor unit activity, in SC at 11.7 ms for 46/66 units and in SCM at 12.7 ms for 51/58 motor units. There were fewer significant responses in the ipsilateral SC and contralateral SCM muscles, and they consisted primarily of weak increases in activity. Surface responses recorded over the contralateral SC were positive-negative during neck rotation, similar to the ipsilateral cervical vestibular evoked myogenic potential in SCM. Responses in SC were present in the patients with hearing loss and absent in the patient with vestibular loss, confirming their vestibular origin. The results describe a pattern of inhibition consistent with the synergistic relationship between these muscles for axial head rotation, with the crossed vestibular projection to the contralateral SC being weaker than the ipsilateral projection to the SCM. NEW & NOTEWORTHY We used acoustic vestibular stimulation to investigate the saccular projections to the splenius capitis (SC) and sternocleidomastoid (SCM) muscles in humans. Single motor unit recordings from within the muscles demonstrated strong inhibitory projections to the contralateral SC and ipsilateral SCM muscles and weak excitatory projections to the opposite muscle pair. This synergistic pattern of activation is consistent with a role for the reflex in axial rotation of the head.


2015 ◽  
Vol 36 (4) ◽  
pp. 746-753 ◽  
Author(s):  
Courtney C. J. Voelker ◽  
Amelia Lucisano ◽  
Dorina Kallogjeri ◽  
Belinda C. Sinks ◽  
Joel A. Goebel

2003 ◽  
Vol 13 (2-3) ◽  
pp. 131-141 ◽  
Author(s):  
Claire C. Gianna-Poulin ◽  
Valerie Stallings ◽  
F. Owen Black

This study assessed the eye movement responses to active head rotation in six subjects with complete unilateral vestibular loss (UVL), five subjects with posterior canal plugging (PCP) and age- and sex-matched normal subjects. Subjects performed head rotations in the pitch and yaw planes at frequencies ranging from 2 to 6 Hz, while looking at an earth-fixed target. Vertical eye movement gains obtained in UVL, PCP and normal subjects were not significantly different. Vertical phases decreased with increasing head movement frequencies in both UVL and PCP subjects. Although this decrease produced significantly different vertical phases between UVL and normal subjects for head movements above 3.9 Hz, vertical phases in some normal subjects were similar to those obtained in UVL subjects. We conclude that active head oscillations in the pitch plane are not clinically useful for the detection of vertical canal impairment limited to one ear. As expected, UVL subjects showed reduced horizontal gains, and eye velocity asymmetries during active head rotation in the yaw plane. Results in some PCP subjects suggested possible minor impairments of horizontal vestibulo-ocular reflexes.


2002 ◽  
Vol 12 (1) ◽  
pp. 35-45 ◽  
Author(s):  
Krister Brantberg ◽  
Arne Tribukait

In recent years it has been demonstrated that loud clicks generate short latency vestibular evoked myogenic potentials (VEMP). It has also been demonstrated that midline forehead skull tap stimulation evokes similar VEMP. In the present study, the influence of skull tap direction on VEMP was studied in 13 normal subjects and in five patients with unilateral vestibular loss. Gentle skull taps were delivered manually above each ear on the side of the skull. The muscular responses were recorded over both sternocleidomastoid muscles using skin electrodes. Among the normals, laterally directed skull taps evoked “coordinated contraction-relaxation responses”, i.e. skull taps on one side evoked a negative-positive “inverted” VEMP on that side and a positive-negative "normal" VEMP on the other side. Among patients with unilateral vestibular function loss, skull taps above the lesioned ear evoked similar coordinated contraction-relaxation responses. However, skull taps above the healthy ear did not evoke that type of response. These findings suggest that laterally directed skull taps activate mainly the contralateral labyrinth.


1996 ◽  
Vol 76 (6) ◽  
pp. 4009-4020 ◽  
Author(s):  
S. T. Aw ◽  
T. Haslwanter ◽  
G. M. Halmagyi ◽  
I. S. Curthoys ◽  
R. A. Yavor ◽  
...  

1. The kinematics of the human angular vestibuloocular reflex (VOR) in three dimensions was investigated in 12 normal subjects during high-acceleration head rotations (head “impulses”). A head impulse is a passive, unpredictable, high-acceleration (3,000–4,000 degrees/s2) head rotation of approximately 10–20 degrees in roll, pitch, or yaw, delivered with the subject in the upright position and focusing on a fixation target. Head and eye rotations were measured with dual search coils and expressed as rotation vectors. The first of these two papers describes a vector analysis of the three-dimensional input-output kinematics of the VOR as two indexes in the time domain: magnitude and direction. 2. Magnitude is expressed as speed gain (G) and direction as misalignment angle (delta). G is defined as the ratio of eye velocity magnitude (eye speed) to head velocity magnitude (head speed). delta is defined as the instantaneous angle by which the eye rotation axis deviates from perfect alignment with the head rotation axis in three dimensions. When the eye rotation axis aligns perfectly with the head rotation axis and when eye velocity is in a direction opposite to head velocity, delta = 0. The orientation of misalignment between the head and the eye rotation axes is characterized by two spatial misalignment angles, which are the projections of delta onto two orthogonal coordinate planes that intersect at the head rotation axis. 3. Time series of G were calculated for head impulses in roll, pitch, and yaw. At 80 ms after the onset of an impulse (i.e., near peak head velocity), values of G were 0.72 +/- 0.07 (counterclockwise) and 0.75 +/- 0.07 (clockwise) for roll impulses, 0.97 +/- 0.05 (up) and 1.10 +/- 0.09 (down) for pitch impulses, and 0.95 +/- 0.06 (right) and 1.01 +/- 0.07 (left) for yaw impulses (mean +/- 95% confidence intervals). 4. The eye rotation axis was well aligned with head rotation axis during roll, pitch, and yaw impulses: delta remained almost constant at approximately 5–10 degrees, so that the spatial misalignment angles were < or = 5 degrees. delta was 9.6 +/- 3.1 (counterclockwise) and 9.0 +/- 2.6 (clockwise) for roll impulses, 5.7 +/- 1.6 (up) and 6.1 +/- 1.9 (down) for pitch impulses, and 6.2 +/- 2.2 (right) and 7.9 +/- 1.5 (left) for yaw impulses (mean +/- 95% confidence intervals). 5. VOR gain (gamma) is the product of G and cos(delta). Because delta is small in normal subjects, gamma is not significantly different from G. At 80 ms after the onset of an impulse, gamma was 0.70 +/- 0.08 (counterclockwise) and 0.74 +/- 0.07 (clockwise) for roll impulses, 0.97 +/- 0.05 (up) and 1.09 +/- 0.09 (down) for pitch impulses, and 0.94 +/- 0.06 (right) and 1.00 +/- 0.07 (left) for yaw impulses (mean +/- 95% confidence intervals). 6. VOR latencies, estimated with a latency shift method, were 10.3 +/- 1.9 (SD) ms for roll impulses, 7.6 +/- 2.8 (SD) ms for pitch impulses, and 7.5 +/- 2.9 (SD) ms for yaw impulses. 7. We conclude that the normal VOR produces eye rotations that are almost perfectly compensatory in direction as well as in speed, but only during yaw and pitch impulses. During roll impulses, eye rotations are well aligned in direction, but are approximately 30% slower in speed.


2005 ◽  
Vol 94 (5) ◽  
pp. 3417-3429 ◽  
Author(s):  
Mark F. Walker ◽  
David S. Zee

L. W. Schultheis and D. A. Robinson showed that the axis of the rotational vestibuloocular reflex (RVOR) cannot be altered by visual-vestibular mismatch (“cross-axis adaptation”) when the vestibulocerebellum is lesioned. This suggests that the cerebellum may calibrate the axis of eye velocity of the RVOR under natural conditions. Thus we asked whether patients with cerebellar disease have alterations in the RVOR axis and, if so, what might be the mechanism. We used three-axis scleral coils to record head and eye movements during yaw, pitch, and roll head impulses in 18 patients with cerebellar disease and in a comparison group of eight subjects without neurologic disease. We found distinct shifts of the eye-velocity axis in patients. The characteristic finding was a disconjugate upward eye velocity during yaw. Measured at 70 ms after the onset of head rotation, the median upward gaze velocity was 15% of yaw head velocity for patients and <1% for normal subjects ( P < 0.001). Upward eye velocity was greater in the contralateral (abducting) eye during yaw and in the ipsilateral eye during roll. Patients had a higher gain (eye speed/head speed) for downward than for upward pitch (median ratio of downward to upward gain: 1.3). In patients, upward gaze velocities during both yaw and roll correlated with the difference in anterior (AC) and posterior canal excitations, scaled by the respective pitch gains. Our findings support the hypothesis that upward eye velocity during yaw results from AC excitation, which must normally be suppressed by the intact cerebellum.


2007 ◽  
Vol 98 (1) ◽  
pp. 295-302 ◽  
Author(s):  
Mark F. Walker ◽  
Jing Tian ◽  
David S. Zee

We studied the effect of cerebellar lesions on the 3-D control of the rotational vestibuloocular reflex (RVOR) to abrupt yaw-axis head rotation. Using search coils, three-dimensional (3-D) eye movements were recorded from nine patients with cerebellar disease and seven normal subjects during brief chair rotations (200°/s2 to 40°/s) and manual head impulses. We determined the amount of eye-position dependent torsion during yaw-axis rotation by calculating the torsional-horizontal eye-velocity axis for each of three vertical eye positions (0°, ±15°) and performing a linear regression to determine the relationship of the 3-D velocity axis to vertical eye position. The slope of this regression is the tilt angle slope. Overall, cerebellar patients showed a clear increase in the tilt angle slope for both chair rotations and head impulses. For chair rotations, the effect was not seen at the onset of head rotation when both patients and normal subjects had nearly head-fixed responses (no eye-position-dependent torsion). Over time, however, both groups showed an increasing tilt-angle slope but to a much greater degree in cerebellar patients. Two important conclusions emerge from these findings: the axis of eye rotation at the onset of head rotation is set to a value close to head-fixed (i.e., optimal for gaze stabilization during head rotation), independent of the cerebellum and once the head rotation is in progress, the cerebellum plays a crucial role in keeping the axis of eye rotation about halfway between head-fixed and that required for Listing's Law to be obeyed.


1981 ◽  
Vol 90 (3) ◽  
pp. 241-245 ◽  
Author(s):  
Masahiro Takahashi ◽  
Takuya Uemura ◽  
Takehisa Fujishiro

Compensatory eye movement and gaze fixation during active head rotation were studied in patients with unilateral and bilateral loss of vestibular function. Patients with bilateral lesions were asked to perform mental arithmetic tasks in the dark. Although compensatory eye movements of these patients corresponded to 38–46% of compensatory movements in normal subjects, the ability of patients with lesions to visually fix on a stationary target was markedly impaired. Visual fixation on moving targets attached to the head (head-fixed targets) was also measured and found to be good. For patients with unilateral lesions, in the early stages of the disease, findings during rotations to the intact side resembled those for normal subjects, while results of rotations to the affected side resembled those for patients with bilateral lesions.


2020 ◽  
Vol 123 (4) ◽  
pp. 1486-1495 ◽  
Author(s):  
Andrew R. Wagner ◽  
Michael C. Schubert

The study objective was to understand how the contralesional labyrinth contributes to gaze and gait stability after unilateral vestibular deafferentation (UVD). Head impulse testing (vHIT) was completed in 37 individuals [22 women (59%); age 52.13 ± 11.59 yr, mean ± SD] with UVD from vestibular schwannoma resection. Compensatory saccades (CS) and vestibulo-ocular reflex (VOR) gain were analyzed for both ipsilesional and contralesional impulses. Gait speed (10-m walk test) and endurance (2-min walk test) were collected for 35 individuals. CS were recruited during contralesional head rotation regardless of VOR gain on either the ipsilesional [ρ = 0.21 (−0.14, 0.57); Spearman rank (95% confidence interval)] or contralesional side [ρ = −0.04 (−0.42, 0.35)]. Additionally, the latency of these CS (151.19 ± 52.41 ms) was similar to that of CS generated during ipsilesional rotation (165.65 ± 21.62 ms; P = 0.159). CS recruited during ipsilesional vHIT were of a higher velocity ( P < 0.001) and greater frequency ( P < 0.001) compared with contralesional CS. VOR gain asymmetry was significantly correlated with gait speed [ρ = −0.37 (−0.73, −0.01)], yet individual VOR gain was not correlated [ipsilesional: ρ = 0.17 (−0.20, 0.55); contralesional: ρ = −0.18 (−0.52, 0.15)]. Our data reveal CS are recruited at similar latencies without correlation to VOR gain or direction of head rotation, and that the central integration of ipsilesional and contralesional vestibular afference correlates with gait. Together, our data suggest the brain considers vestibular afference from both sides when generating related behavioral output after UVD. NEW & NOTEWORTHY After unilateral vestibular deafferentation, compensatory saccades (CS) have similar latencies regardless of the direction of head rotation, and those CS generated during contralesional head rotation are unrelated to extent of vestibular loss. Additionally, the extent of asymmetry in residual vestibular function, not the extent of vestibular loss, correlates with gait speed. Our data suggest a common mechanism is responsible for the generation of CS and restoration of gait speed in vestibular compensation.


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