Gaze stabilization by optokinetic reflex (OKR) and vestibulo-ocular reflex (VOR) during active head rotation in man

Vestibulo-ocular reflex (VOR)-optokinetic reflex (OKR) interaction was studied in normal human subjects during active sine-like head movements in the horizontal plane for a variety of vestibular-optokinetic stimulus combinations (frequency range, 0.05-1.6 Hz). At low to mid frequencies (< 0.2 Hz) the eyes tended to be stabilized on the optokinetic pattern, independently of whether the head, the pattern, or both were rotated. At higher frequencies, the OKR gain was attenuated and, in each of the differing stimulus combinations, the eyes became increasingly stabilized in space. Qualitatively similar results were obtained when, for the same visual-vestibular combinations, the head was passively rotated at 0.05 and 0.8 Hz. The data could be simulated by a model which assumes a linear interaction of vestibular and optokinetic signals. It considers the OKR with its negative feedback loop of primordial importance for image stabilization on the retina and the VOR only as a useful addition which compensates for the limited bandwidth of the OKR during high frequency/velocity head rotations in a stationary visual environment.     

Gain and delay of human vestibulo-ocular reflexes to oscillation and steps of the head by a reactive torque helmet. I. Normal subjects

Vestibulo-ocular reflexes (VOR) were evaluated with a reactive torque helmet that imposed high-frequency oscillation (2-20 Hz) or step displacements of the head in the horizontal plane. The present paper describes the results in patients with vestibular deficiencies (labyrinthine defective; LD); experimental and analytical techniques and results for normal subjects were described in Part 1 of this paper. The patient groups included: total unilateral LD (related to acoustic neuroma; n = 40); severe (clinically total) bilateral LD (n = 7); bilateral hyporeflexia (n = 14); unilateral hyporeflexia (n = 11); and patients with LD phenomena that had subsided (n = 3). Helmet-induced head steps provided the most specific information. Characteristically, gain was lowered in one direction or both directions after unilateral or bilateral vestibular lesions, respectively; in general, the magnitude of the gain reduction correlated well with the degree of complaints and disability. Surprisingly, delay was systematically prolonged (up to several tens of milliseconds) in all groups of subjects with manifest vestibular pathology. These results suggest that the determination of delay, in addition to gain of the VOR, is feasible and important in the evaluation of vestibular function. The results of head oscillation generally supported the results for steps, but were somewhat less specific. The responses to manually generated head steps roughly agreed with those to helmet-induced steps, but because of the non-uniform acceleration they allowed a less exact analysis of VOR function.     

Rx for hand pieces: preventive maintenance key to long life

Patients with hemispheric lesions frequently suffer from equilibrium impairment that may be prolonged and may interfere with rehabilitation. In an effort to clarify whether this phenomenon is related to vestibular dysfunction, we examined the relationship of the horizontal vestibulo-ocular reflex (VOR) with stability in 15 patients with unilateral hemispheric stroke. The study included electro-oculographic recording of the VOR while the patients were rotated in a vestibular chair. Stability was scored in accordance with the patients' ability to maintain equilibrium in six graded positions. The findings demonstrated relationship between VOR gain (eye/head displacement) and equilibrium. It is suggested that the "loss of balance" after stroke may be related to an impairment of the corticovestibular modulation of the vestibular function.     

Eye movements evoked by proprioceptive stimulation along the body axis in humans

Proprioceptive input arising from torsional body movements elicits small reflexive eye movements. The functional relevance of these eye movements is still unknown so far. We evaluated their slow components as a function of stimulus frequency and velocity. The horizontal eye movements of seven adult subjects were recorded using an infrared device, while horizontal rotations were applied at three segmental levels of the body [i.e., between head and shoulders (neck stimulus), shoulders and pelvis (trunk stimulus), and pelvis and feet (leg stimulus)]. The following results were obtained: (1) Sinusoidal leg stimulation evoked an eye response with the slow component in the direction of the movement of the feet, while the response to trunk and neck stimulation was oriented in the opposite direction (i.e., in that of the head). (2) In contrast, the gain behavior of all three responses was similar, with very low gain at mid- to high frequencies (tested up to 0.4 Hz) but increasing gain at low frequencies (down to 0.0125 Hz). We show that this gain behavior is mainly due to a gain nonlinearity for low angular velocities. (3) The responses were compatible with linear summation when an interaction series was tested in which the leg stimulus was combined with a vestibular stimulus. (4) There was good correspondence of the median gain curves when eye responses were compared with psychophysical responses (perceived body rotation in space; additionally recorded in the interaction series). However, correlation of gain values on a single-trial basis was poor. (5) During transient neck stimulation (smoothed position ramp), the neck response noticeably consisted of two components -- an initial head-directed eye shift (phasic component) followed by a shift in the opposite direction (compensatory tonic component). Both leg and neck responses can be described by one simple, dynamic model. In the model the proprioceptive input is fed into the gaze network via two pathways which differ in their dynamics and directional sign. The model simulates either leg or neck responses by selecting an appropriate weight for the gain of one of the pathways (phasic component). The interaction results can also be simulated when a vestibular path is added. This model has similarities to one we recently proposed for human self-motion perception and postural control. A major difference, though, is that the proprioceptive input to the gaze-stabilizing network is weak (restricted to low velocities), unlike that used for perception and postural control. We hold that the former undergoes involution during ontogenesis, as subjects depend on the functionally more appropriate vestibulo-ocular reflex. Yet, the weak proprioceptive eye responses that remain may have some functional relevance. Their tonic component tends to stabilize the eyes by slowly shifting them toward the primary head position relative to the body support. This applies solely to the earth-horizontal plane in which the vestibular signal has no static sensitivity.     

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.     

Vestibulo-ocular reflex function as measured with the head autorotation test

The vestibulo-ocular reflex (VOR) of 125 healthy subjects was examined over the frequency range of 0.5-5 Hz with the head autorotation test (HART). During the HART the subjects fixated at a steady target while moving their heads horizontally from side to side with increasing frequencies according to auditory signals. The gain was determined as the ratio between the amplitude of the eye and head movements in five frequency bands between 0.5 and 5 Hz. The phase difference between the eye and head movements was determined in both degrees and milliseconds. The ability to reach high-frequency bands was evaluated. The mean gain was close to unity up 5 Hz, when it decreased to 0.91. The mean phase difference showed a lead of approximately 5 degrees at frequencies below 2 Hz, and at frequencies above 2 Hz there was no phase difference within the resolution of the test. The frequency band of 5 Hz was reached by 78% of the subjects, and that of 4 Hz was reached by 94% of the subjects. In summary, the HART is a new approach with which to study VOR function and determine accurately the VOR for healthy subjects. The normal upper frequency limit is 4 Hz in the HART.     

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)     

Quantitative analysis of human walking trajectory on a circular path in darkness

Thirteen normal (eight young and five older) subjects and a patient who was removed left sided acoustic neurinoma were tested to walk blindfolded along circular paths. They were asked to walk completing two revolutions and to stop when they judged they had returned to the initial position with their head faced to the initial directions. Movements of two markers on the subjects head were recorded by three dimensional motion analyzing system (ELITE system) at 50 Hz which allowed us to measure (a) total walked distance, (b) average radius of the trajectory, and (c) cumulative angle of rotation. Eight young subjects were tested on three circles with radii 0.5, 0.9, and 1.15 m, in two conditions (control, and with mental arythmetic), only to clockwise direction. Five older subjects and a patient were tested on a circle of 0.9 m radius in two conditions, but to both directions, counterclockwise and clockwise. Walked trajectories of young subjects were smooth, whereas those of older subjects tended to be polygonal. Young subjects overshot the ideal distance (6.6%) and ideal radius (9.5%), whereas they undershot the ideal angle (5.1%). There was no effect of circle size or condition on these variables. On the other hand, there was a significant effect of condition on average radius in the older group. The performance of older subjects seemed to be affected by the concurrent mental task. Comparing the counterclockwise walk, the older subjects undershot the turning angle much more than the young subjects which suggest deficits in the vestibular function with aging. The patient showed larger radius and smaller angle while she turned to the healthy side (clockwise) than to the affected side (counterclockwise). Lack of unilateral vestibular information seemed to have affected the circular walking trajectory.     

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.     

Neck afferents and muscle sympathetic activity in humans: implications for the vestibulosympathetic reflex

We have shown previously that head-down neck flexion (HDNF) in humans elicits increases in muscle sympathetic nerve activity (MSNA). The purpose of this study was to determine the effect of neck muscle afferents on MSNA. We studied this question by measuring MSNA before and after head rotation that would activate neck muscle afferents but not the vestibular system (i.e., no stimulation of the otolith organs or semicircular canals). After a 3-min baseline period with the head in the normal erect position, subjects rotated their head to the side (approximately 90%) and maintained this position for 3 min. Head rotation was performed by the subjects in both the prone (n = 5) and sitting (n = 6) positions. Head rotation did not elicit changes in MSNA. Average MSNA, expressed as burst frequency and total activity, was 13 +/- 1 and 13 +/- 1 bursts/min and 146 +/-34 and 132 +/- 27 units/min during baseline and head rotation, respectively. There were no significant changes in calf blood flow (2.6 +/- 0.3 to 2.5 +/- 0.3 ml.100 ml-1.min-1, n = 8) and calf vascular resistance (39 +/- 4 to 41 +/- 4 units; n = 8). Heart rate (64 +/- 3 to 66 +/- 3 beats/min; P = 0.058) and mean arterial pressure (90 +/- 3 to 93 +/- 3; P < 0.05) increased slightly during head rotation. Additional neck flexion studies were performed with subjects lying on their side (n = 5), MSNA, heart rate, and mean arterial pressure were unchanged during this maneuver, which also does not engage the vestibular system. HDNF was tested in 9 of the 13 subjects. MSNA was significantly increased by 79 +/- 12% (P < 0.001) during HDNF. These findings indicate that neck afferents activated by horizontal neck rotation or flexion in the absence of significant force development do not elicit changes in MSNA. These findings support the concept that HDNF increases MSNA by the activation of the vestibular system.     

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.     

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.     

Post-ejection thickening as a marker of viable myocardium. An echocardiographic study in patients with chronic coronary artery disease

Useful medical diagnostic information has been reported from low-frequency rotational testing of the horizontal vestibulo-ocular reflex (VOR) of patients with vestibular disorders. Servocontrolled rotating systems have been used as the only practical method to generate stimuli over lower VOR frequency response ranges, the decade from 0.01 to 0.1 Hz. Active head movements have been used for testing the human VOR at higher frequencies, exceeding 0.5 Hz. We examined whether active head movements could be used also to test the VORs of subjects over lower frequency ranges, extending to 0.02 Hz. We used a swept-frequency, active head movement protocol to generate a broad-band stimulus. Eye position was recorded with electro-oculography. Head velocity was recorded with a rotational sensor attached to a head band. Six individual test epochs from human subjects were concatenated to form complex, periodic waveforms of head and eye velocity, 75 seconds in duration. Broad-band cross-spectral signal processing methods were used to compute horizontal VOR system characteristics from these waveforms extending from 0.02 to 2 Hz. The low-frequency VOR data appeared to originate from amplitude modulation of high-frequency active movements, acting as carrier signals. Control experiments and processing of simulated data from a known system excluded the possibility of signal processing artifacts. Results from six healthy subjects showed low-frequency gains and phase values in ranges similar to those from published rotational chair studies of normal subjects. We conclude that it is feasible to test the human VOR over extended low-frequency ranges using active head movements because of amplitude modulation of the head and eye signals.     

Analysis and neural network modeling of the nonlinear correlates of habituation in the vestibulo-ocular reflex

Through the process of habituation, continued exposure to low-frequency (0.01 Hz) rotation in the dark produced suppression of the low-frequency response of the vestibulo-ocular reflex (VOR) in goldfish. The response did not decay gradually, as might be expected from an error-driven learning process, but displayed several nonlinear and nonstationary features. They included asymmetrical response suppression, magnitude-dependent suppression for lower- but not higher-magnitude head rotations, and abrupt-onset suppressions suggestive of a switching mechanism. Microinjection of lidocaine into the vestibulocerebellum of habituated goldfish resulted in a temporary dishabituation. This suggests that the vestibulocerebellum mediates habituation, presumably through Purkinje cell inhibition of vestibular nuclei neurons. The habituated VOR data were simulated with a feed-forward, nonlinear neural network model of the VOR in which only Purkinje cell inhibition of vestibular nuclei neurons was varied. The model suggests that Purkinje cell inhibition may switch in to introduce nonstationarities, and cause asymmetry and magnitude-dependency in the VOR to emerge from the essential nonlinearity of vestibular nuclei neurons.     

Dual adaptation and adaptive generalization of the human vestibulo-ocular reflex

In two experiments, we examined the possibility that the human vestibulo-ocular reflex (VOR) is subject to dual adaptation (the ability to adapt to a sensory rearrangement more rapidly and/or more completely after repeated experience with it) and adaptive generalization (the ability to adapt more readily to a novel sensory rearrangement as a result of prior dual adaptation training). In Experiment 1, the subjects actively turned the head during alternating exposure to a visual-vestibular rearrangement (target/head gain = 0.5) and the normal situation (target/head gain = 0.0). These conditions produced both adaptation and dual adaptation of the VOR but no evidence of adaptive generalization when tested with a target/head gain of 1.0. Experiment 2, in which exposure to the 0.5 gain entailed externally controlled (i.e., passive) whole body rotation, resulted in VOR adaptation but no dual adaptation. As in Experiment 1, no evidence of adaptive generalization was found.     

Kinematic principles of primate rotational vestibulo-ocular reflex. II. Gravity-dependent modulation of primary eye position

The kinematic constraints of three-dimensional eye positions were investigated in rhesus monkeys during passive head and body rotations relative to gravity. We studied fast and slow phase components of the vestibulo-ocular reflex (VOR) elicited by constant-velocity yaw rotations and sinusoidal oscillations about an earth-horizontal axis. We found that the spatial orientation of both fast and slow phase eye positions could be described locally by a planar surface with torsional variation of <2.0 +/- 0.4 degrees (displacement planes) that systematically rotated and/or shifted relative to Listing's plane. In supine/prone positions, displacement planes pitched forward/backward; in left/right ear-down positions, displacement planes were parallel shifted along the positive/negative torsional axis. Dynamically changing primary eye positions were computed from displacement planes. Torsional and vertical components of primary eye position modulated as a sinusoidal function of head orientation in space. The torsional component was maximal in ear-down positions and approximately zero in supine/prone orientations. The opposite was observed for the vertical component. Modulation of the horizontal component of primary eye position exhibited a more complex dependence. In contrast to the torsional component, which was relatively independent of rotational speed, modulation of the vertical and horizontal components of primary position depended strongly on the speed of head rotation (i.e., on the frequency of oscillation of the gravity vector component): the faster the head rotated relative to gravity, the larger was the modulation. Corresponding results were obtained when a model based on a sinusoidal dependence of instantaneous displacement planes (and primary eye position) on head orientation relative to gravity was fitted to VOR fast phase positions. When VOR fast phase positions were expressed relative to primary eye position estimated from the model fits, they were confined approximately to a single plane with a small torsional standard deviation ( approximately 1.4-2.6 degrees). This reduced torsional variation was in contrast to the large torsional spread (well >10-15 degrees ) of fast phase positions when expressed relative to Listing's plane. We conclude that primary eye position depends dynamically on head orientation relative to space rather than being fixed to the head. It defines a gravity-dependent coordinate system relative to which the torsional variability of eye positions is minimized even when the head is moved passively and vestibulo-ocular reflexes are evoked. In this general sense, Listing's law is preserved with respect to an otolith-controlled reference system that is defined dynamically by gravity.     

Quick-freeze deep-etch electron microscopy of the actin-heavy meromyosin complex during the in vitro motility assay

Since mica is a substitute for glass in the in vitro actin motility assay, I examined the structure of heavy meromyosin (HMM) crossbridges supporting actin filaments by quick-freeze deep-etch replica electron microscopy. This method was capable of resolving the inter-domain cleft of the monomeric actin molecule. HMM heads that are not bound to actin, when observed by this technique, were straight and elongated in the absence of ATP but strongly kinked upon addition of ATP or ADP.inorganic vanadate to produce the putative long-lived analog of HMM-ADP.inorganic phosphate. The low-magnification image of the ATP-containing acto-HMM preparation showed features characteristic of sliding actin filaments on glass coverslips. At high magnification, all the HMM molecules were found attached to actin by one head with the majority projecting perpendicular to the filament axis, whereas in the absence of ATP, HMM exhibited two-head binding with a preponderance of molecules tilted at 45 degrees. Detailed examination of the shape of HMM heads involved in sliding showed a rounded, and flat appearance of the tip and comparatively thin neck portion as if the heads grasp actin filament, in contrast to rigor crossbridges which have a pear-shaped configuration with more gradual taper. Such configurations of HMM heads were essentially the same as I observed previously on acto-myosin subfragment-1 (S1) by the same technique, except for the presence of an additional neck portion of HMM which makes interpretaion of the images easier. Interestingly, under actively sliding conditions, very few heads were tilted in the rigor configuration. At first glance, the addition of ADP to the rigor-complex gave images rather like those obtained with ATP, but they turned out to be different. The contribution of the structural change of crossbridges to the force development is discussed.     

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.     

Afferent signals from the extraocular muscles of the pigeon modify the vestibulo-ocular reflex

Although the extraocular muscles (EOM) contain stretch receptors it is generally thought that the afferent signals which they provide play no role in the control of eye movement. We have previously shown that these afferent signals do modify both the vestibular responses of single units in the oculomotor control system and the electromyographic responses of the EOM during the vestibulo-ocular reflex (VOR). We have now investigated the effect of EOM afferent signals on the VOR itself, by recording the electro-oculogram of one eye while imposing movements on the other eye during the VOR. Moving the eye in a manner which mimics the slow phase of the VOR, we have found that, as the peak velocity of the imposed eye movement increases, the amplitude of eye movement of the other eye decreases. These results confirm that the output of the VOR itself, expressed as movement of the globe, and not merely some of its component parts, is modified by EOM afferent signals.