Labyrinthine-defective Subjects Research Articles

Visuo-vestibular Influences on the Moving Platform Locomotor Aftereffect

After walking onto a moving platform subjects experience a locomotor aftereffect (LAE), including a self-generated stumble, when walking again onto a stationary platform. Thus this LAE affords examination of the role of vestibular input during an internally generated postural challenge. The experiments involved walking onto the stationary sled (BEFORE trials), walking onto the moving sled (MOVING), and a second set of stationary trials (AFTER). We investigated 9 bilateral labyrinthine defective subjects (LDS) and 13 age-matched normal controls (NC) with eyes open. We repeated the experiment in 5 NC and 5 LDS but this time the AFTER trials were performed twice, first eyes closed and then on eye reopening. During MOVING trials, LDS were considerably unstable, thus confirming the established role of the vestibular system during externally imposed postural perturbations. During AFTER trials, both groups experienced an aftereffect with eyes open and closed, shown as higher approach gait velocity, a forward trunk overshoot, and increased leg EMG. However, there were no significant group differences due to the fact that stopping the forward trunk overshoot was accomplished by anticipatory EMG bursts. On eye reopening the aftereffect re-emerged, significantly larger in LDS than that in NC. The lack of group differences in AFTER trials suggests that when facing internally generated postural perturbations, as in this adaptation process, the CNS relies less on vestibular feedback and more on anticipatory mechanisms. Reemergence of the aftereffect on eye reopening indicates the existence of a feedforward visuo-contextual mechanism for locomotor learning, which is adaptively enhanced in the absence of vestibular function.

Labyrinthine lesions and motion sickness susceptibility.

The angular vestibulo-ocular reflex (aVOR) has a fast pathway, which mediates compensatory eye movements, and a slow (velocity storage) pathway, which determines its low frequency characteristics and orients eye velocity toward gravity. We have proposed that motion sickness is generated through velocity storage, when its orientation vector, which lies close to the gravitational vertical, is misaligned with eye velocity during head motion. The duration of the misalignment, determined by the dominant time constant of velocity storage, causes the buildup of motion sickness. To test this hypothesis, we studied bilateral labyrinthine-defective subjects with short vestibular time constants but normal aVOR gains for their motion sickness susceptibility. Time constants and gains were taken from rotational responses. Motion sickness was generated by rolling the head while rotating, and susceptibility was assessed by the number of head movements made before reaching intolerable levels of nausea. More head movements signified lower motion sickness susceptibility. Labyrinthine-defective subjects made more head movements on their first exposure to roll while rotating than normals (39.8 +/- 7.2 vs 13.7 +/- 5.5; P < 0.0001). Normals were tested eight times, which habituated their time constants and reduced their motion sickness susceptibility. Combining data from all subjects, there was a strong inverse relationship between time constants and number of head movements (r = 0.94), but none between motion sickness susceptibility and aVOR gains. This provides further evidence that motion sickness is generated through velocity storage, not the direct pathway, and suggests that motion sickness susceptibility can be reduced by reducing the aVOR time constant.

Influence of pitch tilts on the perception of gravity-referenced eye level in labyrinthine defective subjects

We investigate the role of vestibular information in judging the gravity-referenced eye level (i.e., earth-referenced horizon or GREL) during sagittal body tilt whilst seated. Ten bilateral labyrinthine-defective subjects (LDS) and 10 age-matched controls set a luminous dot to their perception of GREL in darkness, with and without arm pointing. Although judgements were linearly influenced by the magnitude of whole-body tilt, results showed no significant difference between LDS and age-matched controls in the subjective GREL accuracy or in the intra-subject variability of judgement. However, LDS performance without arm pointing was related to the degree of vestibular compensation inferred from another postural study performed with the same patients. LDS did not utilize upper limb input during arm pointing movements as a source of graviceptive information to compensate for the vestibular loss. The data suggest that vestibular cues are not of prime importance in GREL estimates in static conditions. The absence of difference between controls and LDS GREL performance, and the correlation between the postural task and GREL accuracy, indicate that somatosensory input may convey as much graviceptive information required for GREL judgements as the vestibular system.

5.3 Body tilt influence on the perceived gravity-referencedeye level in labyrinthine defective subjects

5.3 Body tilt influence on the perceived gravity-referencedeye level in labyrinthine defective subjects

Vestibulo-autonomic control in man: Short- and long-latency vestibular effects on cardiovascular function

We examined the hypothesis that vestibular signals may exert a rapid control on the heart adjusting cardiovascular function to maintain homoestasis during changes in body posture. Short- and long-latency effects of vestibular stimulation on heart rate (HR), systolic blood pressure (SP), diastolic pressure (DP) and digital blood flow (BF) were studied in fourteen normal controls (NC) and nine labyrinthine-defective subjects (LDS) exposed to abrupt head accelerations. Subjects lay supine with their head suspended in a sling whose 'release' was triggered at delays of 170 ms and 570 ms after an R-spike of the ECG. Release caused the head to fall with an acceleration approximately 0.8 g for approximately 140 ms. Three additional NC underwent head drops at 170 ms, 370 ms, 470 ms and 570 ms to determine response latencies with precision. In NC, the short-latency response to head drops timed 170 to 470 ms after an R-spike was to shorten the time to the next R-spike in comparison to pre-drop heartbeat cycles. Drops at 570 ms delay shortened only the succeeding post-stimulus RR-interval. In LDS, head drops timed 170 ms after a heartbeat failed to shorten the ongoing cardiac cycle. For both delays only the succeeding cardiac cycle was significantly shortened. In all subjects, SP rose slightly by approximately 1-3% and BF decreased by 7-24% after 3-4 heartbeats post-drop. The results are evidence for an excitatory vestibulo-cardiac reflex in man which accelerates heart rate at a latency circa 500-600 ms. SP and BF are affected at longer latencies of several heart beats. A delayed increase of heart rate in response to postural challenge may contribute to the autonomic distress experienced by patients with vestibular loss.

Visual motion detection in patients with absent vestibular function

Labyrinthine defective subjects (LDS) experience oscillopsia during head movements due to the absence of the vestibulo-ocular reflex (VOR). The purpose of this study was to compare horizontal and vertical visual motion detection in LDS during (i) body-stationary and (ii) horizontal whole-body oscillation conditions. Twelve LDS and controls detected the onset of drift direction of a grating that moved with accelerating velocity. Thresholds were raised in the patient group in both conditions. The loss of the VOR per se cannot explain raised thresholds in the body-stationary condition nor during whole-body (horizontal) oscillation with vertical grating motion. Findings indicate changes in visual processing that make LDS less sensitive to visual motion. It is postulated that these changes are due to adaptive mechanisms involved to reduce oscillopsia.

Differential effects of labyrinthine dysfunction on distance and direction during blindfolded walking of a triangular path.

While we walk through the environment, we constantly receive inputs from different sensory systems. For us to accomplish a given task, for example to reach a target location, the sensory information has to be integrated to update our knowledge of self-position and self-orientation with respect to the target so that we can correctly plan and perform the remaining trajectory. As has been shown previously, vestibular information plays a minor role in the performance of linear goal-directed locomotion when walking blindfolded toward a previously seen target within a few meters. The present study extends the question of whether vestibular information is a requirement for goal-directed locomotion by studying a more complex task that also involves rotation: walking a triangular path. Furthermore, studying this task provides information about how we walk a given trajectory, how we move around corners, and whether we are able to return to the starting point. Seven young male, five labyrinthine-defective (LD) and five age- and gender-matched control subjects were asked to walk a previously seen triangular path, which was marked on the ground, first without vision (EC) and then with vision (EO). Each subject performed three clockwise (CW) and three counterclockwise (CCW) walks under the EC condition and one CW and CCW walk under the EO condition. The movement of the subjects was recorded by means of a 3D motion analysis system. Analysis of the data showed that LD subjects had, in the EC condition, a significantly larger final arrival error, which was due to increased directional errors during the turns. However, there was no difference between the groups as regards the overall path length walked. This shows that LD subjects were able to plan and execute the given trajectory without vision, but failed to turn correctly around the corners. Hence, the results demonstrate that vestibular information enhances the ability to perform a planned trajectory incorporating whole body rotations when no visual feedback is available.

Perception of slow pitch and roll body tilts in bilateral labyrinthine-defective subjects

The aim of the present study was to examine whether the perception of slow body tilts in total darkness was affected by a complete loss of vestibular function. Four blindfolded bilateral labyrinthine-defective subjects (LDs) and 12 normal subjects (Normals) were seated and immobilized with large straps against the back of a rotating L-shaped platform, and were passively displaced from the upright at 0.05°·s −1 in the pitch and roll dimensions. Subjects were asked to detect the slow change in their body orientation, by indicating as soon as possible the direction of tilt. After a brief period of practice observed for all LDs at the beginning of the session, results showed no significant difference between LDs and Normals in the mean detection threshold recorded for each direction of tilt. The mean perceptual threshold was 4.4 versus 5.1° in the roll dimension, and 6.1 versus 6.1° in the pitch dimension, for the LDs and Normals, respectively. These findings indicate that the accurate perception of body orientation in quasi-static conditions is mainly allowed by somatosensory information rather than by otolithic inputs.

Visual vertigo: symptom assessment, spatial orientation and postural control

Certain patients with balance disorders report a 'visual vertigo' in which their symptoms are provoked or aggravated by specific visual contexts (e.g. supermarkets, driving or movement of objects). In order to determine the causes of visual vertigo (VV), we assessed symptoms, anxiety and the influence of disorienting visual stimuli in 21 such patients. In 17 out of 21 patients, a peripheral vestibular disorder was diagnosed. Sixteen bilateral labyrinthine-defective subjects (LDS) and 25 normal subjects served as controls. Questionnaire assessment showed that the levels of trait anxiety and childhood motion sickness in the three subject groups were not significantly different. Reporting of autonomic symptoms and somatic anxiety was higher than normal in both patient groups but not significantly different between LDS and VV patients. Handicap levels were not different in the two patient groups, but the reporting of vestibular symptoms was higher in the VV than in the LDS group. The experimental stimuli required subjects to set the subjective visual vertical in three visual conditions: total darkness, in front of a tilted luminous frame (rod and frame test) and in front of a large disc rotating in the frontal plane (rod and disc test). Body sway was also measured in four visual conditions: eyes closed, eyes open, facing the tilted frame and during disc rotation. In psychophysical and postural tests, both LDS and VV patients showed: (i) a significant increase in the tilt of the visual vertical both with the static tilted frame and with the rotating disc; and (ii) an increased postural deviation whilst facing the tilted frame and the rotating disc. The ratio between sway path with eyes closed and eyes open (i.e. the stabilizing effect of vision) was increased in the LDS, but not in VV patients, compared with normal subjects. In contrast, the ratio between sway path during disc rotation and sway path during eyes open (i.e. the destabilizing effect of a moving visual stimulus) was increased in the VV patients but not in LDS. Taken together, these data show that VV patients have abnormally large perceptual and postural responses to disorienting visual environments. VV is not related to trait anxiety or a past history of motion sickness. The results indicate that VV emerges in vestibular patients if they have increased visual dependence and difficulty in resolving conflict between visual and vestibulo-proprioceptive inputs. It is argued that treating these patients with visual motion desensitization, e.g. repeated optokinetic stimulation, should be beneficial.

Coriolis-force-induced trajectory and endpoint deviations in the reaching movements of labyrinthine-defective subjects.

When reaching movements are made during passive constant velocity body rotation, inertial Coriolis accelerations are generated that displace both movement paths and endpoints in their direction. These findings directly contradict equilibrium point theories of movement control. However, it has been argued that these movement errors relate to subjects sensing their body rotation through continuing vestibular activity and making corrective movements. In the present study, we evaluated the reaching movements of five labyrinthine-defective subjects (lacking both semicircular canal and otolith function) who cannot sense passive body rotation in the dark and five age-matched, normal control subjects. Each pointed 40 times in complete darkness to the location of a just extinguished visual target before, during, and after constant velocity rotation at 10 rpm in the center of a fully enclosed slow rotation room. All subjects, including the normal controls, always felt completely stationary when making their movements. During rotation, both groups initially showed large deviations of their movement paths and endpoints in the direction of the transient Coriolis forces generated by their movements. With additional per-rotation movements, both groups showed complete adaptation of movement curvature (restoration of straight-line reaches) during rotation. The labyrinthine-defective subjects, however, failed to regain fully accurate movement endpoints after 40 reaches, unlike the control subjects who did so within 11 reaches. Postrotation, both groups' movements initially had mirror image curvatures to their initial per-rotation reaches; the endpoint aftereffects were significantly different from prerotation baseline for the control subjects but not for the labyrinthine-defective subjects reflecting the smaller amount of endpoint adaptation they achieved during rotation. The labyrinthine-defective subjects' movements had significantly lower peak velocity, higher peak elevation, lower terminal velocity, and a more vertical touchdown than those of the control subjects. Thus the way their reaches terminated denied them the somatosensory contact cues necessary for full endpoint adaptation. These findings fully contradict equilibrium point theories of movement control. They emphasize the importance of contact cues in adaptive movement control and indicate that movement errors generated by Coriolis perturbations of limb movements reveal characteristics of motor planning and adaptation in both healthy and clinical populations.

Adaptation to oscillopsia: a psychophysical and questionnaire investigation.

In this study we explore the reasons why patients with bilateral vestibular failure report disparate degrees of oscillopsia. Twelve bilateral labyrinthine-defective (LD) subjects and twelve normal healthy controls were tested using a self- versus visual-motion psychophysical experiment. The LD subjects also completed a questionnaire designed to quantify the severity of handicap caused by oscillopsia. Additional standardized questionnaires were completed to identify the role of personality, personal beliefs and affective factors in adaptation to oscillopsia. During the psychophysical experiment subjects sat on a motorized Barany chair whilst viewing a large-field projected video image displayed on a screen in front of them. The chair and video image oscillated sinusoidally at 1 Hz in counter-phase at variable amplitudes which were controlled by the subject but constrained, so that the net relative motion of the chair and video image always resulted in a sinusoid with a peak velocity of 50 degrees /s. The subject's task was to find the ratio of chair versus video image motion that subjectively produced the 'most comfortable visual image'. Eye movements were recorded during the experiment in order that the net retinal image slip at the point of maximum visual comfort could be measured. The main findings in the LD subjects were that, as a group, they selected lower chair motion amplitude settings to obtain visual comfort than did the normal control subjects. Responses to the questionnaires highlighted considerable variation in reported handicap due to oscillopsia. Greater oscillopsia handicap scores were significantly correlated with a greater external locus of control (i.e. the perception of having little control over one's health). Retinal slip speed was negatively correlated with oscillopsia handicap score so that patients who suffered the greatest retinal slip were those least handicapped by oscillopsia. The results suggest that adaptation to oscillopsia is partly related to the patient's personal attitude to the recovery process and partly associated with the development of tolerance to the movement of images on the retina during self-motion. The latter is likely to be related to previously described changes in visual motion sensitivity in these patients.

Eye movements during torso rotations in labyrinthine-defective subjects

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 degrees, 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.

Importance of the vestibular system in visually induced nausea and self-vection

The objective of this study was to determine the importance, if any, of the non-auditory labyrinth of the inner ear in visually induced nausea and self-vection in subjects exposed to a moving visual field with and without concomitant pitching head movements. Subjects treated were 15 normals, 18 unilateral labyrinthectomies and 6 bilateral labyrinthectomies. The findings show a higher incidence of pseudo-Coriolis induced nausea in normal subjects compared to unilateral and bilateral labyrinthectomized subjects. When the subjects were exposed to the moving visual field only (no head movement), pronounced self-vection occurred in all subjects, but with earlier onset in the bilateral labyrinthine defective subjects as compared to normal and unilateral defective subjects. The subjective intensities of self-vections reported by labyrinth-defectives were much more pronounced as compared to normal subjects, and it is apparent that visual input in these subjects achieves much more importance in maintaining compensatory eye movements, and the gain of neck reflexes is enhanced. The findings that visual stimulation is more effective in producing the disabling effects after labyrinthine destruction could possibly be explained by enhancement of vision after loss of labyrinthine sensory input, and the gain in neck reflexes is also enhanced after labyrinthectomy.

Hyperventilation effect on postural sway

Objective: To examine the effect of voluntary hyperventilation (HV) on postural sway. Design: Crossover controlled, experimental study. Setting: Human movement and balance clinical research unit. Subjects: Four different groups of normal subjects ( n = 6, 6, 7, and 9) and patients with bilateral absence of vestibular function ( n = 9). Intervention: Partial carbon dioxide pressure (tc-P co 2) was measured transcutaneously with surface electrodes. Body sway was measured with a force platform immediately after maximal voluntary HV for 30 to 90 seconds. Recordings were obtained with eyes open and eyes closed, standing on the platform and on foam-rubber, and after head or body movements. Main Outcome Measure: Postural sway. Results: HV increased body sway in all conditions, but the effects were more intense when subjects were standing directly on the platform surface with their eyes closed. Recordings after HV of 30, 60, and 90sec in normal subjects showed that although CO 2 levels were inversely related to the duration of HV, body sway did not increase further. HV also increased sway after active movements by the subjects. The main sway increase was in sway area and mean and maximal deviations but less for mean sway velocity. HV preferentially increased low-frequency sway oscillations. These effects were also present in labyrinthine-defective subjects. Conclusions: HV increases body sway, but the relationship between CO 2 levels and degree of unsteadiness is not linear. The dizziness reported by patients with HV syndrome may be partly caused by objective unsteadiness. The presence of HV-induced unsteadiness in patients with absent vestibular function indicates that the effects of HV are not mediated by the labyrinth.

Effect of otolith dysfunction. Impairment of visual acuity during linear head motion in labyrinthine defective subjects.

Visual symptoms emerging after the loss of vestibular function are usually attributed to the dysfunction of semicircular canal vestibulo-ocular reflexes, as they have been shown to stabilize vision during angular head movements. However, natural head displacements involve both angular and linear motion, and therefore visual instability may occur because of defective otolith-ocular reflexes (OORs) which are the eye movements evoked by linear head acceleration. In this paper, the relationship between OORs and visual acuity during linear head motion was studied in normal subjects and 14 patients with bilateral loss of caloric responses. OORs were elicited in darkness by step acceleration (0.24 g) of the whole body along the interaural axis. Latency, slow phase velocity and asymmetry of the OOR were measured from the desaccaded and averaged electrooculographic trace. Visual acuity was assessed during sinusoidal lateral oscillation of the subject viewing an earth-fixed target, and vice versa with the subject stationary and the target moving at 0.5, 1.0 and 1.5 Hz. The task was to recognize numbers flashing up on a three digit light-emitting diode visual display. Normal subjects had symmetrical OORs with short latencies (< 130 ms). In patients, OORs were either absent (n = 2) or abnormal with asymmetries (n = 8), diminished velocities (n = 4) or prolonged latencies (n = 6). At high frequency oscillation (1.5 Hz), normal subjects invariably recognized more numbers during self-motion compared with target motion, whereas most patients did not. In patients, abnormal dynamic visual acuity was correlated with absent or delayed OOR responses. This is the first demonstration of a functional role of the OORs in that they contribute to visual stabilization during high frequency linear head motion. Bilateral vestibular failure commonly affects the OORs and thereby compromises dynamic visual acuity.

Visually and posturally mediated tilt illusion in Parkinson's disease and in labyrinthine defective subjects

We tested 24 normal subjects, 24 patients with idiopathic Parkinson's disease (PD), and eight patients with bilateral absence of vestibular function (labyrinthine defective [LD] subjects) in their ability to set a straight line to the perceived gravitational vertical (visual vertical). Measurements were taken in static conditions, sitting upright, and lying down on the right side, and during visual background motion at constant angular velocities around the line of sight (roll-motion) in both sitting upright and sideways position. Aims of the study were to determine if the reported increased "visual dependence" in PD was present in a psychophysical task that is independent of motor performance, and to examine the interaction between visual motion and proprioceptive cues in the perception of verticality, in the absence of vestibular function. LD patients showed abnormally large deviations of the visual vertical induced both by lateral body tilt and by visual roll-motion. This suggests that vestibular cues play a significant part in counterbalancing visually and proprioceptive mediated biases on the perception of verticality. In contrast, PD patients were normal in all these tasks indicating that visual dependence in PD is not present at an afferent/perceptual level.

Thresholds for detection of motion direction during passive lateral whole-body acceleration in normal subjects and patients with bilateral loss of labyrinthine function

To investigate the effect of velocity, acceleration, and gradient of acceleration on self-motion perception, thresholds for detection of direction of whole-body interaural acceleration were determined for various stimulus profiles. For acceleration steps, acceleration thresholds at 67% correct detection of motion direction were similar for eight normals (mean 4.84 cm/s 2 (range 2.9–6.3), peak gradient = 22 cm/s 2) and five labyrinthine-defective subjects (mean 5.65 cm/s 2 (4.85–6.6), peak gradient = 25 cm/s 2). Velocity thresholds were 7.93 cm/s for a proportion of correct responses of 73% for normals and 9.67 cm/s for 69% of correct detection for avestibular subjects. For linear and parabolic accelerations, high intersubject variability was observed both among nine normals and three labyrinthine-defective subjects. Mean normal and avestibular subjects' acceleration thresholds for 74% of correct responses were respectively 12.1 cm/s 2 (7.3–20.4) and 16.4 cm/s 2 (13.2–20) for a ramp with gradient of acceleration = 2.8 cm/s 3, 19.2 cm/s 2 (10.4–35.3) and 28.2 cm/s 2 (21.4–32.8) for a ramp with gradient = 7.9 cm/s 3 and 16.7 cm/s 2 (10.5–25) and 20.6 cm/s 2 (18.4–24.2) for a parabola with second derivative = 1.52 cm/s 4. The corresponding velocity thresholds for normals were 21.2 cm/s (5.2–50.3), 22.0 cm/s (7–56.6), and 22.2 cm/s (9.5–43.7). The lowest thresholds were obtained for acceleration steps indicating that a high acceleration gradient facilitates motion perception. For linear and parabolic accelerations, motion perception seemed to follow an integration of acceleration, but a high intersubject variability was observed. For all stimuli, the range of thresholds for normals and avestibular subjects overlapped showing that detection of motion was not a sole prerogative of the otoliths but could also be performed using somatosensory cues.

The perception of head and neck angular displacement in normal and labyrinthine-defective subjects. A quantitative study using a 'remembered saccade' technique.

The detection of horizontal angular displacement of the head or trunk was assessed in 13 normal subjects and three labyrinthine defective patients. Discrete rotational displacements to the whole body (vestibular stimulus, VS), the trunk whilst keeping the head earth-stationary (cervical stimulus, CS) or the head upon the stationary trunk (combined VS+CS in passive and active mode) were delivered. Amplitudes ranged from 10 degrees to 40 degrees with peak velocities from 5 degrees to 40 degrees/s. Response was quantified as saccadic gain (final position of the eye/amplitude of the rotational stimulus) in a 'remembered saccade' task. it was found that normal subjects show different accuracy according to the sensory channel investigated. If stimulus amplitude was limited (20-30 degrees), gain dropped as rotational velocity decreased during VS but not in conditions including cervical stimulation (CS or VS+CS). Responses combining cervical and vestibular stimuli (VS+CS) were closer to unity gain and showed less scatter than isolated VS and CS. In the labyrinthine-defective patients, VS yielded no structured response but all responses involving cervical stimulation were identical to those of normal subjects when analysed both as a function of stimulus amplitude and velocity. Neither in normal nor in labyrinthine-defective subjects were there significant differences in the ability to detect head angular displacement between passive or active head turns (passive or active VS+CS). The following conclusions can be made. (i) 'Remembered saccade' techniques can be used to investigate cervico-vestibular perception. (ii) The 'high pass' characteristic of the response during VS agrees with the dynamic sensitivity of the vestibular nerve signals. Cervical experiments confirmed that neck responses are position-driven (i.e. 'tonic'). (iii) The detection of head turns is only slightly more accurate when vestibular and cervical signals are combined, but the main input controlling this perception is provided by neck afferents. No specific function for 'efference copy' was apparent in these experiments. (iv) There is no significant change for detecting head turns (on the trunk) in labyrinthine-defective patients. (v) The lack of detectable changes in cervical tasks in labyrinthine-defective patients does not support the view that the potentiation of the cervico-ocular reflex (COR) observed in these patients is due to enhanced sensitivity of the neck afferent system.

Human vestibulo-ocular responses to rapid, helmet-driven head movements.

High-frequency head rotations in the 2-20 Hz range and passive, unpredictable head acceleration impulses were produced by a new technique, utilizing a helmet with a torque motor oscillating a mass. Unrestrained head and eye movements were recorded using magnetic sensor coils in a homogeneous magnetic field. In order to analyze the influence of the visual system on the vestibulo-ocular reflex (VOR), we took measurements under three experimental conditions: (1) with a stationary visual target; (2) in total darkness with the subject imagining the stationary target; and (3) with a head-fixed target. The results in 15 healthy subjects were highly consistent. At 2 Hz, VOR gain was near unity; above 2 Hz, VOR gain started to decrease, but this trend reversed beyond 8 Hz, where the gain increased continuously up to 1.1-1.3 at 20 Hz. Phase lag increased with frequency, from a few deg at 2 Hz to about 45 degrees at 20 Hz. Above 2 Hz, VOR gain was not significantly different for the three experimental conditions. Head acceleration impulses produced a VOR with near-unity gain in both directions. We also tested three subjects with clinically total bilateral loss of labyrinthine functions. These labyrinthine-defective subjects showed, in comparison to the normal subjects, strikingly lower gains and much longer delays in the VOR during sinusoidal and step-like head movements. These results suggest that our new torque-driven helmet technique is effective, safe and convenient, enabling the assessment of the VOR at relatively high frequencies where both visual and mental influences are minimized.

Cervico-ocular reflex enhancement in labyrinthine-defective and normal subjects

The cervico-ocular reflex (COR) was elicited in 12 normal and 30 labyrinthine-defective (LD) subjects, lacking a vestibulo-ocular reflex (VOR) in the usual laboratory tests, by sinusoidal horizontal rotation of the body at 30 degrees amplitude and frequencies of 0.1, 0.2 and 0.4 Hz. The head was fixed in space and the eyes were open in total darkness. The gain of the COR was measured by relating the maximum slow phase velocity (MSPV) of the eyes to the maximum input velocity (19, 38 or 75 degrees/s) and by relating the cumulative eye displacement per hemicycle to the peak-to-peak amplitude of 60 degrees. The COR gain was below 0.25 in the normal subjects. In the LD subjects, a clear COR was observed with a gain of about 0.7 (SD 0.3) at 0.1 Hz, decreasing to about 0.4 (SD 0.2) at 0.4 Hz. There was no appreciable phase lag in 11 of the LD subjects. In 17 other LD subjects, the phase lag was close to 0 degrees at 0.1 Hz and increased to about 20-30 degrees at 0.4 Hz. Testing 4 additional normal subjects with the special instruction to attempt fixation of the knee during trunk rotation in the dark, resulted in an enhanced COR showing many "catch-up" saccades with a gain close to unity; the smooth component was also enhanced. The pattern with catch-up saccades was different from the pattern observed in most LD subjects, which closely resembled the normal VOR elicited by sinusoidal rotation. The special instruction to attempt fixation of the knee was also given to one LD subject during stimulation at 0.2 Hz.(ABSTRACT TRUNCATED AT 250 WORDS)