The response of the vestibulosympathetic reflex to linear acceleration in the rat.

The vestibulosympathetic reflex (VSR) increases blood pressure (BP) upon arising to maintain blood flow to the brain. The optimal directions of VSR activation and whether changes in heart rate (HR) are associated with changes in BP are still not clear. We used manually activated pulses and oscillatory linear accelerations of 0.2-2.5 g along the naso-occipital, interaural, and dorsoventral axes in isoflurane-anesthetized, male Long-Evans rats. BP and HR were recorded with an intra-aortic sensor and acceleration with a three-dimensional accelerometer. Linear regressions of BP changes in accelerations along the upward, downward, and forward axes had slopes of ≈3-6 mmHg · g-1 (P < 0.05). Lateral and backward accelerations did not produce consistent changes in BP. Thus upward, downward, and forward translations were the directions that significantly altered BP. HR was unaffected by these translations. The VSR sensitivity to oscillatory forward-backward translations was ≈6-10 mmHg · g-1 at frequencies of ≈0.1 Hz (0.2 g), decreasing to zero at frequencies above 2 Hz (1.8 g). Upward, 70° tilts of an alert rat increased BP by 9 mmHg · g-1 without changes in HR, indicating that anesthesia had not reduced the VSR sensitivity. The similarity in BP induced in alert and anesthetized rats indicates that the VSR is relatively insensitive to levels of alertness and that the VSR is likely to cause changes in BP through modification of peripheral vascular resistance. Thus the VSR, which is directed toward the cardiovascular system, is in contrast to the responses in the alert state that can produce sweating, alterations in BP and HR, and motion sickness.

Reinforcement learning interfaces for biomedical database systems.

Studies of neural function that are carried out in different laboratories and that address different questions use a wide range of descriptors for data storage, depending on the laboratory and the individuals that input the data. A common approach to describe non-textual data that are referenced through a relational database is to use metadata descriptors. We have recently designed such a prototype system, but to maintain efficiency and a manageable metadata table, free formatted fields were designed as table entries. The database interface application utilizes an intelligent agent to improve integrity of operation. The purpose of this study was to investigate how reinforcement learning algorithms can assist the user in interacting with the database interface application that has been developed to improve the performance of the system.

Vestibular control of sympathetic activity. An otolith-sympathetic reflex in humans.

It has been proposed that a vestibular reflex originating in the otolith organs and other body graviceptors modulates sympathetic activity during changes in posture with regard to gravity. To test this hypothesis, we selectively stimulated otolith and body graviceptors sinusoidally along different head axes in the coronal plane with off-vertical axis rotation (OVAR) and recorded sympathetic efferent activity in the peroneal nerve (muscle sympathetic nerve activity, MSNA), blood pressure, heart rate, and respiratory rate. All parameters were entrained during OVAR at the frequency of rotation, with MSNA increasing in nose-up positions during forward linear acceleration and decreasing when nose-down. MSNA was correlated closely with blood pressure when subjects were within +/-90 degrees of nose-down positions with a delay of 1.4 s, the normal latency of baroreflex-driven changes in MSNA. Thus, in the nose-down position, MSNA was probably driven by baroreflex afferents. In contrast, when subjects were within +/-45 degrees of the nose-up position, i.e., when positive linear acceleration was maximal along the naso-ocipital axis, MSNA was closely related to gravitational acceleration at a latency of 0.4 s. This delay is too short for MSNA changes to be mediated by the baroreflex, but it is compatible with the delay of a response originating in the vestibular system. We postulate that a vestibulosympathetic reflex, probably originating mainly in the otolith organs, contributes to blood pressure maintenance during forward linear acceleration. Because of its short latency, this reflex may be one of the earliest mechanisms to sustain blood pressure upon standing.

Orienting otolith-ocular reflexes in the rabbit during static and dynamic tilts and off-vertical axis rotation.

Orienting otolith-ocular reflexes were assessed in rabbits using static tilt, off-vertical axis rotation (OVAR) and sinusoidal oscillation about earth-horizontal axes. In all paradigms, head pitch produced ocular counter-pitch and vergence, and head roll produced ocular counter-roll and conjugate yaw version. Thus, vergence and version are essential components of orienting reflexes along the naso-occipital and bitemporal axes. Vergence and version caused misalignment between the axes of eye and head movement during pitch and roll head movements. Semicircular canal input broadened the band-pass of these orienting reflexes, which would make them more appropriate when compensating for head movement during active motion.

Vestibular compensation and orientation during locomotion.

Body, head, and eye movements were studied in three dimensions while walking and turning to determine the role of the vestibular system in directing gaze and maintaining spatial orientation. The body, head, and eyes were represented as three-dimensional coordinate frames, and the movement of these frames was related to a trajectory frame that described the motion of the body on a terrestrial plane. The axis-angle of the body, head, and eye rotation were then compared to the axis-angle of the rotation of the gravitoinertial acceleration (GIA). We inferred the role of the vestibular system during locomotion and the contributions of the VCR and VOR by examining the interrelationship between these coordinate frames. Straight walking induced head and eye rotations in a compensatory manner to the linear accelerations, maintaining head pointing and gaze along the direction of forward motion. Turning generated a combination of compensation and orientation responses. The head leads and steers the turn while the eyes compensate to maintain stable horizontal gaze in space. Saccades shift horizontal gaze as the turn is executed. The head pitches, as during straight walking. It also rolls so that the head tends to align with the orientation of the GIA. Head orientation changes anticipate orientation changes of the GIA. Eye orientation follows the changes in GIA orientation so that the net orientation gaze is closer to the orientation of the GIA. The study indicates that the vestibular system utilizes compensatory and orienting mechanisms to stabilize spatial orientation and gaze during walking and turning.

The human vestibulo-ocular reflex during linear locomotion.

During locomotion, there is a translation and compensatory rotation of the head in both the vertical and horizontal planes. During moderate to fast walking (100 m/min), vertical head translation occurs at the frequency of stepping (2 Hz) and generates peak linear acceleration of 0.37 g. Lateral head translation occurs at the stride frequency (1 Hz) and generates peak linear acceleration of 0.1 g. Peak head pitch and yaw angular velocities are approximately 17 degrees/s. The frequency and magnitude of these head movements are within the operational range of both the linear and angular vestibulo-ocular reflex (IVOR and aVOR). Vertical eye movements undergo a phase reversal from near to far targets. When viewing a far (>1 m) target, vertical eye velocity is typical of an aVOR response; that is, it is compensatory for head pitch. At close viewing distances (<1 m), vertical eye velocity is in phase with head pitch and is compensatory for vertical head translation, suggesting that the IVOR predominantly generates the eye movement response. Horizontal head movements during locomotion occur at the stride frequency of 1 Hz, where the IVOR gain is low. Horizontal eye movements are compensatory for head yaw at all viewing distances and are likely generated by the aVOR.

Orientation of the eyes to gravitoinertial acceleration.

Orientation of the eyes to gravitoinertial acceleration, i.e., to the sum of gravity and the linear accelerations acting on the head and body, is a basic property of the linear vestibulo-ocular reflex to support vision. Present in a wide range of species from the lateral-eyed rabbit to frontal-eyed monkeys and humans, the eyes deviate in pitch, roll and yaw in response to pitch, roll and yaw head movements. The eyes also converge in response to naso-occipital linear acceleration. This paper provides examples of ocular orientation generated by static tilt and off-vertical axis rotation in three dimensions and demonstrates specifically how vergence would support vision in the rabbit.

Changes in the vestibulo-ocular reflex after plugging of the semicircular canals.

The gain of the angular vestibulo-ocular reflex (aVOR) was determined in monkeys by rotation about a spatial vertical axis while upright or statically tilted forward and backward. Horizontal, vertical, and roll gains were determined at each head orientation and plotted as a function of head tilt. Before canal plugging, animals had maximal (spatial) horizontal gains when upright (spatial phase 0 degrees) and maximal roll gains when tilted forward or backward 90 degrees. Plugging caused striking changes in the characteristics of the aVOR gains at low frequencies. After plugging of the vertical canals, maximal horizontal and roll gains both occurred at head tilts of approximately 30 degrees forward. When the lateral canals were plugged, maximal horizontal and roll responses occurred when the head was tilted back approximately 50 degrees. The aVOR gains of the canal-plugged animals were also affected by stimulus frequency. In every instance, as stimulus frequency increased, the spatial phases shifted toward the normal response, that is, the response before plugging. This normalization effect was observed even in the animals with all six semicircular canals plugged, indicating that normalization was not due to spatial adaptation. A three-dimensional dynamic and kinematic model of the aVOR was able to account for all types of canal plugging by a simple change in the dominant time constant of the plugged canals from 3 s to 5 s to approximately 0.07 s. The model accurately predicted responses of the normal and canal-plugged animals at all frequencies. These data show that the central vestibular system does not spatially adapt to losses resulting from canal plugging.

Perception of tilt (somatogravic illusion) in response to sustained linear acceleration during space flight.

During the 1998 Neurolab mission (STS-90), four astronauts were exposed to interaural and head vertical (dorsoventral) linear accelerations of 0.5 g and 1 g during constant velocity rotation on a centrifuge, both on Earth and during orbital space flight. Subjects were oriented either left-ear-out or right-ear-out (Gy centrifugation), or lay supine along the centrifuge arm with their head off-axis (Gz centrifugation). Pre-flight centrifugation, producing linear accelerations of 0.5 g and 1 g along the Gy (interaural) axis, induced illusions of roll-tilt of 20 degrees and 34 degrees for gravito-inertial acceleration (GIA) vector tilts of 27 degrees and 45 degrees , respectively. Pre-flight 0.5 g and 1 g Gz (head dorsoventral) centrifugation generated perceptions of backward pitch of 5 degrees and 15 degrees , respectively. In the absence of gravity during space flight, the same centrifugation generated a GIA that was equivalent to the centripetal acceleration and aligned with the Gy or Gz axes. Perception of tilt was underestimated relative to this new GIA orientation during early in-flight Gy centrifugation, but was close to the GIA after 16 days in orbit, when subjects reported that they felt as if they were 'lying on side'. During the course of the mission, inflight roll-tilt perception during Gy centrifugation increased from 45 degrees to 83 degrees at 1 g and from 42 degrees to 48 degrees at 0.5 g. Subjects felt 'upside-down' during in-flight Gz centrifugation from the first in-flight test session, which reflected the new GIA orientation along the head dorsoventral axis. The different levels of in-flight tilt perception during 0.5 g and 1 g Gy centrifugation suggests that other non-vestibular inputs, including an internal estimate of the body vertical and somatic sensation, were utilized in generating tilt perception. Interpretation of data by a weighted sum of body vertical and somatic vectors, with an estimate of the GIA from the otoliths, suggests that perception weights the sense of the body vertical more heavily early in-flight, that this weighting falls during adaptation to microgravity, and that the decreased reliance on the body vertical persists early post-flight, generating an exaggerated sense of tilt. Since graviceptors respond to linear acceleration and not to head tilt in orbit, it has been proposed that adaptation to weightlessness entails reinterpretation of otolith activity, causing tilt to be perceived as translation. Since linear acceleration during in-flight centrifugation was always perceived as tilt, not translation, the findings do not support this hypothesis.

Ocular counterrolling induced by centrifugation during orbital space flight.

During the 1998 Neurolab mission (STS-90), four astronauts were exposed to interaural centripetal accelerations (Gy centrifugation) of 0.5 g and 1 g during rotation on a centrifuge, both on Earth and during orbital space flight. Subjects were oriented either left-ear out or right-ear out, facing or back to motion. Binocular eye movements were measured in three dimensions using a video technique. On Earth, tangential centrifugation that produces 1 g of interaural linear acceleration combines with gravity to tilt the gravitoinertial acceleration (GIA) vector 45 degrees in the roll plane relative to the head vertical, generating a summed vector of 1.4 g. Before flight, this elicited mean ocular counterrolling (OCR) of 5.7 degrees. Due to the relative absence of gravity during flight, there was no linear acceleration along the dorsoventral axis of the head. As a result, during in-flight centrifugation, gravitoinertial acceleration was strictly aligned with the centripetal acceleration along the interaural axis. There was a small but significant decrease (mean 10%) in the magnitude of OCR in space (5.1 degrees). The magnitude of OCR during postflight 1 g centrifugation was not significantly different from preflight OCR (5.9 degrees). Findings were similar for 0.5 g centrifugation, but the OCR magnitude was approximately 60% of that induced by centrifugation at 1 g. OCR during pre- and postflight static tilt was not significantly different and was always less than OCR elicited by centrifugation of Earth for an equivalent interaural linear acceleration. In contrast, there was no difference between the OCR generated by in-flight centrifugation and by static tilt on Earth at equivalent interaural linear accelerations. These data support the following conclusions: (1) OCR is generated predominantly in response to interaural linear acceleration; (2) the increased OCR during centrifugation on Earth is a response to the head dorsoventral 1 g linear acceleration component, which was absent in microgravity. The dorsoventral linear acceleration could have activated either the otoliths or body-tilt receptors that responded to the larger GIA magnitude (1.4 g), to generate the increased OCR during centrifugation on Earth. A striking finding was that magnitude of OCR was maintained throughout and after flight. This is in contrast to most previous postflight OCR studies, which have generally registered decreases in OCR. We postulate that intermittent exposure to artificial gravity, in the form of the centripetal acceleration experienced during centrifugation, acted as a countermeasure to deconditioning of this otolith-ocular orienting reflex during the 16-day mission.

Interaction of the body, head, and eyes during walking and turning.

Body, head, and eye movements were measured in five subjects during straight walking and while turning corners. The purpose was to determine how well the head and eyes followed the linear trajectory of the body in space and whether head orientation followed changes in the gravito-inertial acceleration vector (GIA). Head and body movements were measured with a video-based motion analysis system and horizontal, vertical, and torsional eye movements with video-oculography. During straight walking, there was lateral body motion at the stride frequency, which was at half the frequency of stepping. The GIA oscillated about the direction of heading, according to the acceleration and deceleration associated with heel strike and toe flexion, and the body yawed in concert with stepping. Despite the linear and rotatory motions of the head and body, the head pointed along the forward motion of the body during straight walking. The head pitch/roll component appeared to compensate for vertical and horizontal acceleration of the head rather than orienting to the tilt of the GIA or anticipating it. When turning corners, subjects walked on a 50-cm radius over two steps or on a 200-cm radius in five to seven steps. Maximum centripetal accelerations in sharp turns were ca.0.4 g, which tilted the GIA ca.21 degrees with regard to the heading. This was anticipated by a roll tilt of the head of up to 8 degrees. The eyes rolled 1-1.5 degrees and moved down into the direction of linear acceleration during the tilts of the GIA. Yaw head deviations moved smoothly through the turn, anticipating the shift in lateral body trajectory by as much as 25 degrees. The trunk did not anticipate the change in trajectory. Thus, in contrast to straight walking, the tilt axes of the head and the GIA tended to align during turns. Gaze was stable in space during the slow phases and jumped forward in saccades along the trajectory, leading it by larger angles when the angular velocity of turning was greater. The anticipatory roll head movements during turning are likely to be utilized to overcome inertial forces that would destabilize balance during turning. The data show that compensatory eye, head, and body movements stabilize gaze during straight walking, while orienting mechanisms direct the eyes, head, and body to tilts of the GIA in space during turning.

Context-specific adaptation of the vertical vestibuloocular reflex with regard to gravity.

We determined whether head position with regard to gravity is an important context for angular vestibuloocular reflex (aVOR) gain adaptation. Vertical aVOR gains were adapted with monkeys upright or on side by rotating the animals about an interaural axis in phase or out of phase with the visual surround for 4 h. When aVOR gains were adapted with monkeys upright, gain changes were symmetrical when tested in either on-side position (23 +/- 7%; mean +/- SD). After on-side adaptation, however, gain changes were always larger when animals were tested in the same on-side position in which they were adapted. Gain changes were 43 +/- 16% with ipsilateral side down and 9 +/- 8% with contralateral side down. The context-specific effects of head position on vertical aVOR gain were the same whether the gain was increased or decreased. The data indicate that vertical aVOR gain changes are stored in the context of the head orientation in which changes were induced. This association could be an important context for expressing the adapted state of the aVOR gain during vertical head movement.

Promethazine affects optokinetic but not vestibular responses in monkeys.

BACKGROUND: Promethazine is used to treat motion sickness including Space Adaptation Syndrome, but there is incomplete information about how it affects vestibular and optokinetic responses. METHODS: Vestibular and optokinetic nystagmus, recorded with eye coils, were characterized in monkeys after administration of promethazine at dosages approximately equivalent to those used by humans in space. RESULTS: The initial increase of horizontal eye velocity during optokinetic nystagmus (OKN) was reduced after receiving the drug. Consequently, it took a longer time for eye velocity to rise to 60% of steady state value, the normal initial jump in eye velocity. Steady state OKN, maximum gains of optokinetic after-nystagmus (OKAN) and OKAN falling time constants were unaffected. The gains and time constants of the horizontal, vertical and roll angular vestibulo-ocular reflex (aVOR), the amplitude and velocity of saccades, and ocular counter-rolling (OCR), induced by off-vertical axis rotation (OVAR) were unaffected by promethazine. A two-component optokinetic model simulated the data simply by reducing the gain of the initial (rapid) component of OKN. A reduction in coupling between a non-linear element and the velocity storage integrator was required to simulate some vertical OKN data. CONCLUSIONS: Promethazine reduces the gain of the direct visual-oculomotor pathway in monkeys. It has little effect on saccades, the gain and time constant of the aVOR and the low frequency linear vestibulo-ocular reflex (IVOR), which orients the eyes during ocular counterrolling. The optokinetic deficit is consistent with reported reduction in ocular pursuit and VOR suppression after promethazine in humans.

Role of muscle pulleys in producing eye position-dependence in the angular vestibuloocular reflex: a model-based study.

It is well established that the head and eye velocity axes do not always align during compensatory vestibular slow phases. It has been shown that the eye velocity axis systematically tilts away from the head velocity axis in a manner that is dependent on eye-in-head position. The mechanisms responsible for producing these axis tilts are unclear. In this model-based study, we aimed to determine whether muscle pulleys could be involved in bringing about these phenomena. The model presented incorporates semicircular canals, central vestibular pathways, and an ocular motor plant with pulleys. The pulleys were modeled so that they brought about a rotation of the torque axes of the extraocular muscles that was a fraction of the angle of eye deviation from primary position. The degree to which the pulleys rotated the torque axes was altered by means of a pulley coefficient. Model input was head velocity and initial eye position data from passive and active yaw head impulses with fixation at 0 degrees, 20 degrees up and 20 degrees down, obtained from a previous experiment. The optimal pulley coefficient required to fit the data was determined by calculating the mean square error between data and model predictions of torsional eye velocity. For active head impulses, the optimal pulley coefficient varied considerably between subjects. The median optimal pulley coefficient was found to be 0.5, the pulley coefficient required for producing saccades that perfectly obey Listing's law when using a two-dimensional saccadic pulse signal. The model predicted the direction of the axis tilts observed in response to passive head impulses from 50 ms after onset. During passive head impulses, the median optimal pulley coefficient was found to be 0.21, when roll gain was fixed at 0.7. The model did not accurately predict the alignment of the eye and head velocity axes that was observed early in the response to passive head impulses. We found that this alignment could be well predicted if the roll gain of the angular vestibuloocular reflex was modified during the initial period of the response, while pulley coefficient was maintained at 0.5. Hence a roll gain modification allows stabilization of the retinal image without requiring a change in the pulley effect. Our results therefore indicate that the eye position-dependent velocity axis tilts could arise due to the effects of the pulleys and that a roll gain modification in the central vestibular structures may be responsible for countering the pulley effect.

Functions of the nucleus of the optic tract (NOT). I. Adaptation of the gain of the horizontal vestibulo-ocular reflex.

We studied the role of the nucleus of the optic tract (NOT) in adapting the gain of the angular vestibulo-ocular reflex (aVOR) in rhesus and cynomolgus monkeys using lesions and temporary inactivation with muscimol. The aVOR gain was adaptively reduced by forced sinusoidal rotation (0.25 Hz, 60 degrees/s) in a self-stationary visual surround, i.e., a visual surround that moved with the subject, or by wearing x0.5 reducing lenses during natural head movements. The aVOR gains dropped by 20-30% after 2 h and by about 30% after 4 h. Muscimol injections caused a loss of adaptation of contraversive-eye velocities induced by the aVOR, and their gains promptly returned to or above preadapted levels. The gains of the adapted ipsiversive and vertical eye velocities produced by the aVOR were unaffected by muscimol injections. Lesions of NOT significantly reduced or abolished the animals' ability to adapt the gain of contraversive aVOR-induced eye velocities, and the monkeys were unable to suppress these contraversive-eye velocities in a self-stationary surround. The lesions did not affect ipsiversive aVOR-induced eye velocities, and the animals were still able to suppress them. Lesions of NOT also affected the unadapted or "default" aVOR gains. After unilateral NOT lesions, gains of ipsiversive aVOR-induced eye velocity were reduced, while gains of contraversive aVOR-induced eye velocity were either unaffected or slightly increased. Consistent with this, muscimol injections into the NOT of unadapted monkeys slightly reduced the gains of ipsiversive and increased the gains of contraversive-eye velocities by about 8-10%. We conclude that each NOT processes ipsiversive retinal-slip information about visual surround movement relative to the head induced by the aVOR. In the presence of visual surround movement, the retinal-slip signal is suppressed, leading to adaptive changes in the gain of aVOR-induced contraversive horizontal eye velocities. NOT also has a role in controlling and maintaining the current state of the aVOR gains. Thus, it plays a unique role in producing and supporting adaptation of the gain of the horizontal aVOR that is likely to be important for stabilizing gaze during head movement. Pathways through the inferior olive are presumably important for this adaptation.

Functions of the nucleus of the optic tract (NOT). II. Control of ocular pursuit.

Ocular pursuit in monkeys, elicited by sinusoidal and triangular (constant velocity) stimuli, was studied before and after lesions of the nucleus of the optic tract (NOT). Before NOT lesions, pursuit gains (eye velocity/target velocity) were close to unity for sinusoidal and constant-velocity stimuli at frequencies up to 1 Hz. In this range, retinal slip was less than 2 degrees. Electrode tracks made to identify the location of NOT caused deficits in ipsilateral pursuit, which later recovered. Small electrolytic lesions of NOT reduced ipsilateral pursuit gains to below 0.5 in all tested conditions. Pursuit was better, however, when the eyes moved from the contralateral side toward the center (centripetal pursuit) than from the center ipsilaterally (centrifugal pursuit), although the eyes remained in close proximity to the target with saccadic tracking. Effects of lesions on ipsilateral pursuit were not permanent, and pursuit gains had generally recovered to 60-80% of baseline after about 2 weeks. One animal had bilateral NOT lesions and lost pursuit for 4 days. Thereafter, it had a centrifugal pursuit deficit that lasted for more than 2 months. Vertical pursuit and visually guided saccades were not affected by the bilateral NOT lesions in this animal. We also compared effects of these and similar NOT lesions on optokinetic nystagmus (OKN) and optokinetic after-nystagmus (OKAN). Correlation of functional deficits with NOT lesions from this and previous studies showed that rostral lesions of NOT in and around the pretectal olivary nucleus, which interrupted cortical input through the brachium of the superior colliculus (BSC), affected both smooth pursuit and OKN. In two animals in which it was tested, NOT lesions that caused a deficit in pursuit also decreased the rapid and slow components of OKN slow-phase velocity and affected OKAN. It was previously shown that slightly more caudal NOT lesions were more effective in altering gain adaptation of the angular vestibulo-ocular reflex (aVOR). The present findings suggest that cortical pathways through rostral NOT play an important role in maintenance of ipsilateral ocular pursuit. Since lesions that affected ocular pursuit had similar effects on ipsilateral OKN, processing for these two functions is probably closely linked in NOT, as it is elsewhere.

Effect of viewing distance on the generation of vertical eye movements during locomotion.

Vertical head and eye coordination was studied as a function of viewing distance during locomotion. Vertical head translation and pitch movements were measured using a video motion analysis system (Optotrak 3020). Vertical eye movements were recorded using a video-based pupil tracker (Iscan). Subjects (five) walked on a linear treadmill at a speed of 1.67 m/s (6 km/h) while viewing a target screen placed at distances ranging from 0.25 to 2.0 m at 0. 25-m intervals. The predominant frequency of vertical head movement was 2 Hz. In accordance with previous studies, there was a small head pitch rotation, which was compensatory for vertical head translation. The magnitude of the vertical head movements and the phase relationship between head translation and pitch were little affected by viewing distance, and tended to orient the naso-occipital axis of the head at a point approximately 1 m in front of the subject (the head fixation distance or HFD). In contrast, eye velocity was significantly affected by viewing distance. When viewing a far (2-m) target, vertical eye velocity was 180 degrees out of phase with head pitch velocity, with a gain of 0. 8. This indicated that the angular vestibulo-ocular reflex (aVOR) was generating the eye movement response. The major finding was that, at a close viewing distance (0.25 m), eye velocity was in phase with head pitch and compensatory for vertical head translation, suggesting that activation of the linear vestibulo-ocular reflex (lVOR) was contributing to the eye movement response. There was also a threefold increase in the magnitude of eye velocity when viewing near targets, which was consistent with the goal of maintaining gaze on target. The required vertical lVOR sensitivity to cancel an unmodified aVOR response and generate the observed eye velocity magnitude for near targets was almost 3 times that previously measured. Supplementary experiments were performed utilizing body-fixed active head pitch rotations at 1 and 2 Hz while viewing a head-fixed target. Results indicated that the interaction of smooth pursuit and the aVOR during visual suppression could modify both the gain and phase characteristics of the aVOR at frequencies encountered during locomotion. When walking, targets located closer than the HFD (1.0 m) would appear to move in the same direction as the head pitch, resulting in suppression of the aVOR. The results of the head-fixed target experiment suggest that phase modification of the aVOR during visual suppression could play a role in generating eye movements consistent with the goal of maintaining gaze on targets closer than the HFD, which would augment the lVOR response.

Model-based study of the human cupular time constant.

The time constant of the angular vestibulo-ocular reflex (aVOR), measured from the response to steps of rotation about a yaw axis, has frequently been estimated as a single exponential. However, the slow phase velocity envelope during per- or post-rotatory nystagmus is more accurately represented by two exponential modes. One represents activity in the vestibular nerve induced by deflection of the cupula, the other by activation that the input from the canals produces in the central velocity storage integrator. The sum of the cupula and the integrator responses describes the overall response of slow phase eye velocity and can be approximated by a double exponential. Frequently, there is a plateau in the initial portion of eye velocity response, but this may be masked by habituation, making the cupula contribution unobservable and impossible to estimate. Using a model-based technique to analyze responses with a clear plateau, we estimated peripheral and central vestibular time constants by double exponential fits to slow phase eye velocity. Cupular time constants were varied from 1 to 10 s to identify values that gave optimal fits of the data according to a Chi-square criterion. The mean cupular time constant for 10 human subjects was 4.2 +/- 0.6 s. Fits of the data were also good for time constants between 3.5 to 7 s, but not for 1 to 3 or 7.5 to 10 s. The estimated cupular time constants also fit responses where there was no plateau. In 8 monkeys, cupular time constants were estimated as 3.9 +/- 0.5 s, which agreed with those derived from activity in the vestibular nerve. There was no difference between monkey and human cupular time constants from these estimates. It is likely that the human cupular time constant is similar to that of the monkey and shorter than previously thought.