Changes in dorsal neck muscle activity related to imposed eye movement in the decerebrate pigeon

Movements of the head and eyes are known to be intimately related. Eye position has also been shown to be closely related to the electromyographic activity of dorsal neck muscles; however, extraocular muscle proprioception has not generally been considered to play a part in the control of such movements. We have previously shown that, in the pigeon, imposed movements of one eye modify the vestibular responses of several dorsal neck muscles in ways that are dependent on stimulus parameters such as the amplitude and velocity of imposed eye movement. The present study examines more closely the interactions between imposed eye movements and different muscle pairs. The three neck muscle pairs studied each responded to afferent signals from the extraocular muscles in discrete and specific ways which appeared to be correlated with their different actions. Complementary effects of imposed eye movements in the horizontal plane were seen for both the complexus and splenius muscle pairs, with imposed eye movements in one direction producing the largest inhibition of the ipsilateral muscle's vestibular response and imposed eye movements in the opposite direction the largest inhibition of the contralateral muscle's vestibular response. During roll tilt oscillation (ear-up/ear-down) in the frontal plane, similar complementary effects of imposed eye movement were seen in the complexus muscle pair, but the splenius muscle pair showed little tuning, with similar inhibition for imposed eye movement directed either upwards or downwards. In contrast to these complementary effects, the biventer cervicis muscle pair showed no vestibular modulation during vestibular stimulation in the horizontal plane and their spontaneous activity was not altered by imposed eye movement. During roll-tilt oscillation (ear-up/ear-down) in the frontal plane imposed eye movement directed vertically upwards increased both muscles' vestibular responses and imposed eye movement directed vertically downwards inhibited both muscles' vestibular responses. Section of the ophthalmic branch of the trigeminal nerve (deafferenting the eye muscles) abolished the effects of imposed eye movement on the neck muscle pairs. In conjunction with further control experiments these results provide compelling evidence that proprioceptive signals from the extraocular muscles reach the neck muscles and provide them with a functionally significant signal. We have previously shown that signals from the extraocular muscles appear to be involved in the control of the vestibulo-ocular reflex. It follows from the experiments reported here that proprioceptive signals from the extraocular muscles are also likely to be involved in the control of gaze.     

Disturbed eye movements after whiplash due to injuries to the posture control system

Self-reports after whiplash often indicate associations with vertigo and reading problems. Neuropsychological and otoneurological tests were applied to a group of whiplash patients (n = 26) and to a carefully matched control group. The whiplash group deviated from the control group on measures of eye movements during reading, on smooth pursuit eye movements with the head in normal position, and with the body turned to the left or to the right. Clinical, caloric, and neurophysiological tests showed no injury to the vestibular system or to the CNS. Test results suggest that injuries to the neck due to whiplash can cause distortion of the posture control system as a result of disorganized neck proprioceptive activity.     

Torticollis due to disinhibition of the vestibulo-collic reflex in a patient with Steele-Richardson-Olszewski syndrome

A patient with the clinical picture of Steele-Richardson-Olszewski syndrome and an unusual intermittent neck twisting is reported. He had virtually no voluntary ocular movements and only very slow, low-amplitude voluntary head movements. However, in response to optokinetic or vestibular stimulation, he developed full eye deviations in the direction of the slow phase of the expected nystagmus. No quick phases were observed, and the deviation outlasted the duration of the vestibular stimuli because of defective saccades. The head also turned fully during these stimuli, quicker than on attempted voluntary movements, and remained deviated similarly to the eyes. This suggests that the neck deviations in this patient were due to a disinhibited vestibulo-collic reflex and a disturbed head position resetting mechanism. Neck electromyographic responses in response to whole-body rotation indicated that the vestibulocollic reflex responsible for the torticollis in this patient had a short latency of approximately 30 ms.     

Vestibular and somatosensory contributions to responses to head and body displacements in stance

The relative contribution of vestibular and somatosensory information to triggering postural responses to external body displacements may depend on the task and on the availability of sensory information in each system. To separate the contribution of vestibular and neck mechanisms to the stabilization of upright stance from that of lower body somatosensory mechanisms, responses to displacements of the head alone were compared with responses to displacements of the head and body, in both healthy subjects and in patients with profound bilateral vestibular loss. Head displacements were induced by translating two 1-kg weights suspended on either side of the head at the level of the mastoid bone, and body displacements were induced translating the support surface. Head displacements resulted in maximum forward and backward head accelerations similar to those resulting from body displacements, but were not accompanied by significant center of body mass, ankle, knee, or hip motions. We tested the effect of disrupting somatosensory information from the legs on postural responses to head or body displacements by sway-referencing the support surface. The subjects' eyes were closed during all testing to eliminate the effects of vision. Results showed that head displacements alone can trigger medium latency (48-84 ms) responses in the same leg and trunk muscles as body displacements. Nevertheless, it is unlikely that vestibular signals alone normally trigger directionally specific postural responses to support surface translations in standing humans because: (1) initial head accelerations resulting from body and head displacements were in opposite directions, but were associated with activation of the same leg and trunk postural muscles; (2) muscle responses to displacements of the head alone were only one third of the amplitude of responses to body displacements with equivalent maximum head accelerations; and (3) patients with profound bilateral vestibular loss showed patterns and latencies of leg and trunk muscle responses to body displacements similar to those of healthy subjects. Altering somatosensory information, by sway-referencing the support surface, increased the amplitude of ankle muscle activation to head displacements and reduced the amplitude of ankle muscle activation to body displacements, suggesting context-specific reweighting of vestibular and somatosensory inputs for posture. In contrast to responses to body displacements, responses to direct head displacements appear to depend upon a vestibulospinal trigger, since trunk and leg muscle responses to head displacements were absent in patients who had lost vestibular function as adults.(ABSTRACT TRUNCATED AT 400 WORDS)     

Human horizontal vestibulo-ocular reflex initiation: effects of acceleration, target distance, and unilateral deafferentation

The vestibulo-ocular reflex (VOR) generates compensatory eye movements in response to angular and linear acceleration sensed by semicircular canals and otoliths respectively. Gaze stabilization demands that responses to linear acceleration be adjusted for viewing distance. This study in humans determined the transient dynamics of VOR initiation during angular and linear acceleration, modification of the VOR by viewing distance, and the effect of unilateral deafferentation. Combinations of unpredictable transient angular and linear head rotation were created by whole body yaw rotation about eccentric axes: 10 cm anterior to eyes, centered between eyes, centered between otoliths, and 20 cm posterior to eyes. Subjects viewed a target 500, 30, or 15 cm away that was extinguished immediately before rotation. There were four stimulus intensities up to a maximum peak acceleration of 2,800 degrees/s2. The normal initial VOR response began 7-10 ms after onset of head rotation. Response gain (eye velocity/head velocity) for near as compared with distant targets was increased as early as 1-11 ms after onset of eye movement; this initial effect was independent of linear acceleration. An otolith mediated effect modified VOR gain depending on both linear acceleration and target distance beginning 25-90 ms after onset of head rotation. For rotational axes anterior to the otoliths, VOR gain for the nearest target was initially higher but later became less than that for the far target. There was no gain correction for the physical separation between the eyes and otoliths. With lower acceleration, there was a nonlinear reduction in the early gain increase with close targets although later otolith-mediated effects were not affected. In subjects with unilateral vestibular deafferentation, the initial VOR was quantitatively normal for rotation toward the intact side. When rotating toward the deafferented side, VOR gain remained less than half of normal for at least the initial 55 ms when head acceleration was highest and was not modulated by target distance. After this initial high acceleration period, gain increased to a degree depending on target distance and axis eccentricity. This behavior suggests that the commissural VOR pathways are not modulated by target distance. These results suggest that the VOR is initially driven by short latency ipsilateral target distance dependent and bilateral target-distance independent canal pathways. After 25 ms, otolith inputs contribute to the target distance dependent pathway. The otolith input later grows to eventually dominate the target distance mediated effect. When otolith input is unavailable the target distance mediated canal component persists. Modulation of canal mediated responses by target distance is a nonlinear effect, most evident for high head accelerations.     

Evaluation of vestibular and visual oculomotor function

The visual system interacts synergistically with the vestibular system. A normally functioning vestibulo-ocular reflex is necessary but not sufficient for optimum visual acuity during head motion. Studies of dynamic visual acuity, the acuity achieved during relative motion of visual targets or of the observer, indicate that motion of images on the retina markedly compromises vision. The vestibulo-ocular reflex normally provides a substantial measure of stabilization of the retina during head movements, but purely vestibular compensatory eye movements are not sufficiently precise for optimal vision under all circumstances. Other mechanisms, including visual tracking, motor preprogramming, prediction, and mental set, interact synergistically to optimize the gain (eye velocity divided by head velocity) of compensatory head movements. All of these mechanisms are limited in their capacity to produce effective visual-vestibular interaction at higher rotational frequencies and velocities. It is under these conditions that vestibular deficits give rise to symptoms of oscillopsia. Patients having vestibular lesions exploit mechanisms of visual-vestibular interaction to compensate by substitution for deficient vestibular function. Thus, for accurate topographic clinical diagnosis of vestibular lesions, testing conditions should isolate purely vestibular responses. This may be done by testing reflex eye movements during passively generated rotations in darkness, or perhaps by testing during other types of motion under conditions of extreme frequency and velocity sufficient to attenuate the effects of visual-vestibular interaction. This article reviews clinical tests of vestibular function in relation to synergistic interactions with vision.     

Voluntary head stabilization in space during oscillatory trunk movements in the frontal plane performed in weightlessness

The ability voluntarily to stabilize the head in space during lateral rhythmic oscillations (0.59+/-0.09 Hz) of the trunk has been investigated during microgravity (microG) and normal gravity (nG) conditions (parabolic flights). Five healthy young subjects, who gave informed consent, were examined. The movements were performed with eyes open or eyes closed, during phases of either microG or nG. The main result was that head orientation with respect to vertical may be stabilized about the roll axis under microG with, as well as without vision, despite the reduction in vestibular afferent and muscle proprioceptive inputs. Moreover, the absence of head stabilization about the yaw axis confirms that the degrees of freedom of the neck can be independently controlled, as was previously reported. These results seem to indicate that voluntary head stabilization does not depend crucially upon static vestibular afferents. Head stabilization in space may in fact be organized on the basis of either dynamic vestibular afferents or a short-term memorized postural body schema.     

Tectal codification of eye movements in goldfish studied by electrical microstimulation. f

This work compares the tectal codification of eye movements in goldfish with those reported for other vertebrate groups. Focal electrical stimulation was applied in various tectal zones and the characteristics of evoked eye movements were examined as a function of (i) the position of the stimulation over the tectal surface, (ii) the initial position of the eyes and (iii) the parameters (pulse rate, current strength, duration) of the stimulus. In a large medial zone, stimulation within the intermediate and deep layers of the tectum evoked contraversive saccades of both eyes, whose direction and amplitude were roughly congruent with the retinotopic representation of the visual world within overlying layers. These saccades were minimally influenced by the initial position of the eye in the orbit. The topographical arrangement of evoked saccades and body movements suggests that this tectal zone triggers orienting responses in a similar way to those described in other vertebrates. Stimulations applied within the caudal tectum also evoked contraversive saccades, but in disagreement with the overlying retinotopic map--the vertical component was absent. Taken together with electrically evoked body movements reported in free-swimming fish, these saccades could reveal that this zone is involved in escape responses. When stimulations were applied within the anteromedial zone of the tectum, contraversive movements of both eyes appeared much more dependent on initial eye position. Saccades elicited from this area displayed characteristics of "goal-directed saccades" which were similar to those described in the cat. The generation of goal-directed movements from the anteromedial zone suggests that this portion of the goldfish optic tectum has a different intrinsic organization or is connected with the brainstem saccade generator in a different fashion than the medial zone. Finally, stimulation of the extreme anteromedial zone evoked convergent eye movements. These movements and those reported in free-swimming fish following electrical stimulation of this tectal area suggest that this zone could be involved in feeding responses. The relationships between the parameters of electrical stimulation and the characteristics of elicited saccades suggest that the stimulated location within the tectum determines a constant direction in the evoked saccade, whereas the amount and duration of tectal activity, as mimicked by changes in stimulus parameters, together with the tectal locus, determine the velocity and amplitude of the evoked saccade.     

Assessment of vestibular function by videonystagmoscopy

Videonystagmoscopy has been used to subjectively observe the responses of the vestibular system in a population of patients with vestibular deficits. These results were compared with those of a control group of healthy, age-matched volunteers. The videonystagmoscopy device is made of one or two CCD cameras mounted on lightproof goggles, allowing a subjective observation of ocular movements on a video monitor. The eye movements, as well as the position of the head in space, can be recorded on videotape. The eyes are illuminated by infrared light emitting diodes placed on each side of the camera lens. The subjects are seated on a manually driven Barany chair. Subjects went through a protocol of passive roll head tilt on each side, followed by a slow, whole body rotation of 180 degrees amplitude, clockwise and counterclockwise, and then a head shaking test (HST). The eyes were subjectively observed, and we focussed on: torsional eye movements during head tilt, nystagmus when the rotation had stopped, and nystagmus induced by HST. With this simple and noninvasive examining procedure, screening of vestibular function at the bedside or during E.N.T. clinical investigations is possible.     

Cervicocephalic kinesthetic sensibility, active range of cervical motion, and oculomotor function in patients with whiplash injury

OBJECTIVE: To investigate cervicocephalic kinesthetic sensibility, active range of cervical motion, and oculomotor function in patients with whiplash injury. DESIGN: A 2-year review of consecutive patients admitted to the emergency unit after whiplash injury. SETTING: An otorhinolaryngology department. PATIENTS AND SUBJECTS: Twenty-seven consecutive patients with diagnosed whiplash injury (14 men and 13 women, mean age, 33.8yrs [range, 18 to 66yrs]). The controls were healthy subjects without a history of whiplash injury. MAIN OUTCOME MEASURES: Oculomotor function was tested at 2 months and at 2 years after whiplash injury. The ability to appreciate both movement and head position was studied. Active range of cervical motion was measured. Subjective intensity of neck pain and major medical symptoms were recorded. RESULTS: Active head repositioning was significantly less precise in the whiplash subjects than in the control group. Failures in oculomotor functions were observed in 62% of subjects. Significant correlations occurred between smooth pursuit tests and active cervical range of motion. Correlations also were established between the oculomotor test and the kinesthetic sensibility test. CONCLUSION: The results suggest that restricted cervical movements and changes in the quality of proprioceptive information from the cervical spine region affect voluntary eye movements. A flexion/extension injury to the neck may result in dysfunction of the proprioceptive system. Oculomotor dysfunction after neck trauma might be related to cervical afferent input disturbances.     

Eye-head coordination in labyrinthine-defective humans

Eye-head coordination during saccadic gaze shifts normally relies on vestibular information. A vestibulo-saccadic reflex (VSR) is thought to reduce the eye-in-head saccade to account for current head movement, and the vestibulo-ocular reflex (VOR) stabilizes postsaccadic gaze while the head movement is still going on. Acute bilateral loss of vestibular function is known to cause overshoot of gaze saccades and postsaccadic instability. We asked how patients suffering from chronic vestibular loss adapt to this situation. Eye and head movements were recorded from six patients and six normal control subjects. Subjects tracked a random sequence of horizontal target steps, with their heads (1) fixed in primary position, (2) free to move, or (3) preadjusted to different head-to-target offsets (to provoke head movements of different amplitudes). Patients made later and smaller head movements than normals and accepted correspondingly larger eye eccentricities. Targeting accuracy, in terms of the mean of the signed gaze error, was better in patients than in normals. However, unlike in normals, the errors of patients exhibited a large scatter and included many overshoots. These overshoots cannot be attributed to the loss of VSR because they also occurred when the head was not moving and were diminished when large head movements were provoked. Patients' postsaccadic stability was, on average, almost as good as that of normals, but the individual responses again showed a large scatter. Also, there were many cases of inappropriate postsaccadic slow eye movements, e.g., in the absence of concurrent head movements, and correction saccades, e.g., although gaze was already on target. Performance in patients was affected only marginally when large head movements were provoked. Except for the larger lag of the head upon the eye, the temporal coupling of eye and head movements in patients was similar to that in normals. Our findings show that patients with chronic vestibular loss regain the ability to make functionally appropriate gaze saccades. We assume, in line with previous work, three main compensatory mechanisms: a head movement efference copy, an active cervico-ocular reflex (COR), and a preprogrammed backsliding of the eyes. However, the large trial-to-trial variability of targeting accuracy and postsaccadic stability indicates that the saccadic gaze system of patients does not regain the high precision that is observed in normals and which appears to require a vestibular head-in-space signal. Moreover, this variability also permeates their gaze performance in the absence of head movements.     

Functional characterization of primary vestibular afferents in the frog

1. In order to more accurately identify the nature of the vestibular input to central neurons, the response properties of single semicircular canal and otolith units in the frog VIIth nerve were studied in curarized preparations. 2. An equation describing the response plane was calculated for each canal on the basis of null point measurements. These results show that the ipsilateral canal planes are orthogonal within 2-5 degrees, and the pairs of right-left synergists are essentially coplanar. A head position of 10-20 degrees maxilla nose up produces optimal horizontal canal and minimal vertical canal activation with horizontal rotation. 3. The frequency response of the horizontal canal was examined in the range 0.025-0.5 Hz. Comparatively shorter phase-lags and a 10 fold greater acceleration gain in this frequency range distinguish the frog from the mammalian species studied. 4. Otolithic responses were tonic, phasic-tonic, and phasic in nature. The preponderance of the latter two groups is stressed (94%). Tonic responses were proportional to the gravitational vector change. Phasic responses were proportional to velocity during transitions in head position and phase-led displacement (30-80%) with sinusoidal acceleration in roll and pitch. 5. Efferent vestibular neurons respond to rotation in the horizontal (usually Type III) as well as vertical planes. Responses in the vertical planes result from canal and/or otolithic input to these neurons indicating that the vestibular efferent system receives extensive multi-labyrinthine convergence.     

Deficits in vertical and torsional eye movements after uni- and bilateral muscimol inactivation of the interstitial nucleus of Cajal of the alert monkey

The mesencephalic interstitial nucleus of Cajal (iC) is considered the neural integrator for vertical and torsional eye movements and has also been proposed to be involved in saccade generation. The aim of this study was to elucidate the function of iC in neural integration of different types of eye movements and to distinguish eye movement deficits due to iC impairment from that of the immediately adjacent rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF). We addressed the following questions: (1) According to the neural integrator hypothesis, all eye movements including the saccadic system and the vestibulo-ocular reflex (VOR) share a common neural integrator. Do iC lesions impair gaze-holding function for vertical and torsional eye positions and the torsional and vertical VOR gain to a similar degree? (2) What are the dynamic properties of vertical and torsional eye movements deficits after iC lesions, e.g., the specificity of torsional and vertical nystagmus? (3) Is iC involved in saccade generation? We performed 13 uni- and three bilateral iC inactivations by muscimol microinjections in four alert monkeys. Three-dimensional eye movements were studied under head-stationary conditions during vertical and torsional VOR. Under static conditions, unilateral iC injections evoked a shift of Listing's plane to the contralesional side (up to 20 degrees), which increased (ipsilesional ear down) or decreased (ipsilesional ear up) by additional static vestibular stimulation in the roll plane, i.e., ocular counterroll was preserved. The monkeys showed a spontaneous torsional nystagmus with a profound downbeat component. The fast phases of torsional nystagmus always beat toward the lesion side (ipsilesional). Pronounced gaze-holding deficit for torsional and vertical eye positions (neural integrator failure) was reflected by the reduction of time constants of the exponential decay of the slow phase to 330-370 ms. Whereas the vertical oculomotor range was profoundly decreased (up to 50%) and vertical saccades were reduced in amplitude, saccade velocity remained normal and horizontal eye movements were not affected. Bilateral iC injections reduced the shift of Listing's plane caused by unilateral injections, i.e., back toward the plane of zero torsion. Torsional nystagmus reversed its direction and ceased, whereas vertical nystagmus persisted. In contrast to unilateral injection, there was additional upbeating nystagmus. Time constants of the position integrator of the gaze-holding system did not differ between unilateral and bilateral injections. The range of stable vertical eye positions and saccade amplitude was smaller when compared with unilateral injections, but the main sequence remained normal. Dynamic vestibular stimulation after unilateral iC injections had virtually no effect on torsional and vertical VOR gain and phase at the same time when time constants already indicated severe integrator failure. Torsional VOR elicited a constant slow-phase velocity offset up to 30 degrees toward the contralesional side, i.e., in the opposite direction to spontaneous torsional nystagmus. Likewise, vertical VOR showed a velocity offset in an upward direction, i.e., opposite to the spontaneous downbeat nystagmus. Contralesional torsional and upward vertical quick phases were missing or severely reduced in amplitude but showed normal velocity. In contrast, bilateral iC injections reduced the gain of the torsional and vertical VOR by 50% and caused a phase lead of 10-20 degrees (eye compared with head velocity). We propose that the slow-phase velocity offset during torsional and vertical VOR reflects a vestibular imbalance. It therefore appears likely that the vertical and torsional nystagmus after iC lesions is not only caused by a neural integrator failure but also by a vestibular imbalance. Unilateral iC injections have clearly differential effects on the VOR and the gaze-holding function. (ABSTRACT TRUNCATED)     

Phenotype, cytokine production and cytolytic capacity of fresh (uncultured) tumour-infiltrating T lymphocytes in human renal cell carcinoma

Abnormalities in the vestibulo-ocular reflex (VOR) after unilateral vestibular injury may cause symptomatic gaze instability. We compared five subjects who had unilateral vestibular lesions with normal control subjects. Gaze stability and VOR gain were measured in three axes using scleral magnetic search coils, in light and darkness, testing different planes of rotation (yaw and pitch), types of stimulus (sinusoids from 0.8 to 2.4 Hz, and transient accelerations) and methods of rotation (active and passive). Eye velocity during horizontal tests reached saturation during high-velocity/acceleration ipsilesional rotation. Rapid vertical head movements triggered anomalous torsional rotation of the eyes. Gaze instability was present even during active rotation in the light, resulting in oscillopsia. These abnormal VOR responses are a consequence of saturating nonlinearities, which limit the usefulness of frequency-domain analysis of rotational test data in describing these lesions.     

From balance regulation to body orientation: two goals for muscle proprioceptive information processing?

This study was based on the assumption that the central processing of proprioceptive inputs that arise from numerous muscles contributes to both awareness and control of body posture. The muscle-spindle inputs form a "proprioceptive chain" which functionally links the eye muscles to the foot muscles. Here, we focused on the specific contribution of two links in the control of human erect posture by investigating how proprioceptive messages arising from ankle and neck muscles may be integrated by the central nervous system. Single or combined mechanical vibrations were applied to different muscle tendons at either one (ankle or neck) or both (ankle plus neck) body levels. The amplitude and the specific direction of the resulting oriented body tilts were analyzed by recording the center of foot pressure (CoP) through a force platform with four strain gauges. The results can be summarized as follows: (1) the vibration-induced whole-body tilts were oriented according to the muscles stimulated; furthermore, the tilts were in opposite directions when neck or ankle muscles on the same side of the body were stimulated; (2) except for the ankle antagonist muscles, co-vibrating adjacent or antagonist muscles at the same body level (ankle or neck) resulted in body sways, whose orientation was a combination of those obtained by stimulating these muscles separately; and (3) likewise, co-vibrating ankle and neck muscles induced whole-body postural responses, whose direction and amplitude were a combination of those obtained by separate vibration. We conclude that the multiple proprioceptive inputs originating from either one or both body levels may be co-processed in terms of vector-addition laws. Moreover, we propose that proprioceptive information from ankle and neck muscles may be used for two tasks: balance control and body orientation, with central integration of both tasks.     

Vestibular-evoked electromyographic responses in soleus: a comparison between click and galvanic stimulation

The aim of this study was to demonstrate, if possible, vestibulospinal reflex responses in soleus using a stimulus known to be capable of exciting vestibular afferents, namely 100-dB (NHL) clicks. We were able to show short-latency electromyographic (EMG) responses after clicks in five of eight normal subjects, and then we compared these responses with those after transmastoid galvanic stimulation (12 normal subjects). Stimulation of the side towards which the head was rotated (i.e. the side facing backwards) with either clicks or the cathode (anode applied to the opposite side) gave an initial excitatory response in soleus, while click or cathodal stimulation of the opposite side (i.e. the side facing forwards) gave an initial inhibitory response. Onset latencies and modulation with changes in postural task were identical for both click- and galvanic-evoked responses. In addition, there was a significant correlation between the amplitudes of the responses in soleus after click and galvanic stimulation (R2=0.72). These similarities suggest that the earliest reflex responses in soleus after clicks and galvanic stimulation may be mediated by a common central pathway. In contrast, there was no correlation between the amplitudes of responses evoked by 100-dB clicks in soleus and those evoked by the same stimulus in the sternocleidomastoid. We conclude that vestibular activation by clicks can evoke reflex responses in lower-limb muscles and these responses have similar characteristics to the earliest responses evoked by galvanic vestibular stimulation.     

Disruption of the Saccharomyces cerevisiae YAP3 gene reduces the proteolytic degradation of secreted recombinant human albumin

In real-life situations, such as during locomotion, or while driving a vehicle, it is necessary to maintain visual fixation and tracking in the presence of the visual flow of the surroundings, which represents a potentially adequate stimulus for the elicitation of optokinetic nystagmus. The present study is concerned with the influence of vestibular disorders, whether pathological or experimentally induced, on those cortically controlled fixation mechanisms, predominantly in the smooth pursuit system, which are involved in suppressing optokinetic information. The study examines the possibility of obtaining an objective measure to assist in counselling patients with unilateral vestibular loss on their vehicle driving ability. To this end, the influence of optokinetic and vestibular stimulation on the execution of smooth pursuit target tracking was measured by recording eye movements during a combination of standard pursuit tasks (0.25, 0.5 and 1 Hz sinusoidal) against standard optokinetic striped backgrounds (0, 30 and 60 degrees/sec). The influence of vestibular imbalance, induced in healthy subjects (n = 35) by unilateral caloric irrigation, and caused by unilateral vestibular loss (in five patients), was also examined under these conditions. During induced vestibular imbalance in normal subjects, and to a greater extent in the tested patients, significant deficits in smooth pursuit gain and increases in saccade frequency were observed during target pursuit against an optokinetic background. Moreover, the findings indicate that the most sensitive parameter for the influence of vestibular optokinetic stimuli on smooth pursuit is frequency of saccades, rather than the gain factor. The tests described here are appropriate for clinical and medico-legal assessment of the influence of vestibular disorder on vehicle driving.     

Selective ablation of immature blood vessels in established human tumors follows vascular endothelial growth factor withdrawal

In the guinea pig, lateral deviation of the head is a cardinal symptom of the vestibular syndrome caused by unilateral labyrinthectomy. In the course of recovery from this syndrome (vestibular compensation), lateral deviation of the head disappears completely in 2-3 days. Because this symptom is known to be due to the lesion of the horizontal semicircular canal system, and since obliquus capitis inferior (OCI) muscle is activated predominantly by yaw rotation (horizontal vestibulocollic reflex), we hypothesized that changes in the activity of this muscle could be at least in part responsible for the lateral head deviation caused by unilateral labyrinthectomy. In order to test this hypothesis, electromyographic (EMG) activities of the right and left OCI muscles, as well as eye movements, were recorded in 12 head-fixed alert guinea pigs at various times after left surgical labyrinthectomy (performed with the animals under halothane anesthesia). After the operation, a decrease in tonic EMG activity was observed in the right (contralateral to the lesion) OCI muscle while an increase in tonic EMG activity was detected in the left (ipsilateral) OCI muscle. In addition, phasic changes in EMG activity associated with ocular nystagmic beats occurred in the OCI muscles. These phasic changes were in the opposite direction to those of the tonic changes. There were bursts of activity in the right OCI and pauses in the left OCI. From measurements of rectified averaged EMG activities which took into account both parts (tonic and phasic) of the phenomenon, it was concluded that the labyrinthectomy-induced asymmetry between the activities of the left and right OCI muscles was high enough and lasted long enough to be an important mechanism in the lateral deviation of the head caused by unilateral labyrinthectomy.     

Interactions between vestibular and proprioceptive inputs triggering and modulating human balance-correcting responses differ across muscles

Interactions between proprioceptive and vestibular inputs contributing to the generation of balance corrections may vary across muscles depending on the availability of sensory information at centres initiating and modulating muscle synergies, and the efficacy with which the muscle action can prevent a fall. Information which is not available from one sensory system may be obtained by switching to another. Alternatively, interactions between sensory systems and the muscle to which this interaction is targeted may be fixed during neural development and not switchable. To investigate these different concepts, balance corrections with three different sets of proprioceptive trigger signals were examined under eyes-open and eyes-closed conditions in the muscles of normal subjects and compared with those of subjects with bilateral peripheral vestibular loss. The different sets of early proprioceptive inputs were obtained by employing three combinations of support surface rotation and translation, for which ankle inputs were nulled, normal or enhanced, the knees were either locked or in flexion, and the trunk was either in flexion or extension. Three types of proprioceptive and vestibulospinal interactions were identified in muscles responses. These interactions were typified by the responses of triceps surae, quadriceps, and paraspinal muscles. The amplitudes of stretch responses at 50 ms after the onset of ankle flexion in triceps surae muscles were related to the velocity of ankle stretch. The amplitude of balance-correcting responses at 100 ms corresponded more with stretch of the biarticular gastrocnemius when the knee was re-extended at 60 ms. Absent stretch reflexes at 50 ms in triceps surae with nulled ankle inputs caused a minor, 12-ms delay in the onset of balance-correcting responses in triceps surae muscles. Vestibular loss caused no change in the amplitude of balance-correcting responses, but a negligible decrease in onset latency in triceps surae even with nulled ankle inputs. Stretch responses in quadriceps at 80 ms increased with the velocity of knee flexion but were overall lower in amplitude in vestibular loss subjects. Balance-correcting responses in quadriceps had amplitudes which were related to the directions of initial trunk movements, were still present when knee inputs were negligible and were also altered after vestibular loss. Stretch and unloading responses in paraspinals at 80 ms were consistent with the direction of initial trunk flexion and extension. Subsequent balance-correcting responses in paraspinals were delayed 20 ms in onset and altered in amplitude by vestibular loss. The changes in the amplitudes of ankle (tibialis anterior), knee (quadriceps) and trunk (paraspinal) muscle responses with vestibular loss affected the amplitudes and timing of trunk angular velocities, requiring increased stabilizing tibialis anterior, paraspinal and trapezius responses post 240 ms as these subjects attempted to remain upright. The results suggest that trunk inputs provide an ideal candidate for triggering balance corrections as these would still be present when vestibular, ankle and knee inputs are absent. The disparity between the amplitudes of stretch reflex and automatic balance-correcting responses in triceps surae and the insignificant alteration in the timing of balance-correcting responses in these muscles with nulled ankle inputs indicates that ankle inputs do not trigger balance corrections. Furthermore, modulation of balance corrections normally performed by vestibular inputs in some but not all muscles is not achieved by switching to another sensory system on vestibular loss. We postulate that a confluence of trunk and upper-leg proprioceptive input establishes the basic timing of automatic, triggered balance corrections which is then preferentially weighted by vestibular modulation in muscles that prevent falling. (ABSTRACT TRUNCATED)     

Effects of the GABA agonists baclofen and THIP on long-term compensation in hemilabyrinthectomised rats

Horizontal eye movements, elicited by sinusoidal rotation in darkness, were recorded with a magnetic search coil technique in pigmented rats, hemilabyrinthectomised 8-12 weeks before the investigation. Separate gains during rotation towards the lesioned side (LS) and the intact side (IS) were calculated by a computer program, demonstrating an asymmetry. Systemic single administration of the GABAB agonist baclofen caused a dose-related temporary rebalancing of the compensatory eye movements to the LS and the IS. At an optimal dose of 14 micromol/kg b.wt symmetry was achieved by excitation of eye movements during rotation to the LS and depression during rotation to the IS. Administration of the GABAA agonist THIP did not obviously reduce the asymmetry. It is suggested that stimulation of GABAB receptors modifies the tonic imbalance between the bilateral vestibular nuclei and/or the central processing of the input from the peripheral sensory organs.