Passive Head Research Articles

Eye-head coordination in darkness: Formulation and testing of a mathematical model

Passive head rotation in darkness produces vestibular nystagmus, consisting of slow and quick phases. The vestibulo-ocular reflex produces the slow phases, in the compensatory direction, while the fast phases, in the same direction as head rotation, are of saccadic origin. We have investigated how the saccadic components of the ocular motor responses evoked by active head rotation in darkness are generated, assuming the only available sensory information is that provided by the vestibular system. We recorded the eye and head movements of nine normal subjects during active head rotation in darkness. Subjects were instructed to rotate their heads in a sinusoidal-like manner and to focus their attention on producing a smooth head rotation. We found that the desired eye position signal provided to the saccadic mechanism by the vestibular system may be modeled as a linear combination of head velocity and head displacement information. Here we present a mathematical model for the generation of both the slow and quick phases of vestibular nystagmus based on our findings. Simulations of this model accurately fit experimental data recorded from subjects.

The use of an implantable loop recorder in the investigation of unexplained syncope in older people.

Reveal is a patient activated implantable loop recorder device with an 18 month battery life now available to assist in the diagnosis of suspected syncope or arrhythmias. We present our experience using this device in older subjects referred to a dedicated falls and syncope clinic in whom usual clinical assessment had not satisfactorily identified an attributable diagnosis but where we still suspected a cardiovascular cause for syncope or falls. during the past 3 years 15 subjects (mean age 73 years, range 61-89 years) had Reveal implanted for symptoms of syncope alone (n=6; 40%) and unexplained falls (n=3; 20%) or symptoms of syncope and unexplained falls (n=6; 40%). Symptom duration was long (mean 48 months; range 4-200 months). Subjects had experienced significant morbidity, 6 subjects (40%) required A&E attendance or hospital admission and 4 (27%) experienced a fracture. Despite extensive and repeated investigations, which included 12-lead ECG, echocardiogram, 24-h ambulatory heart rate monitor, 24-h ambulatory blood pressure monitor, orthostatic blood pressure measurement, supine and erect carotid sinus massage, electroencephalogram, and passive and GTN head up tilt testing, the attributable diagnosis remained unexplained. Of the 15 subjects, 7 have activated the device at 4 (range 0-14) months after implantation. Bradycardia was identified in 3 and ventricular tachycardia in 1 subject. Two subjects did not activate the device during the 18 months it was in-situ. Four people had problems with device activation. This is comparable to rates noted using Reveal in younger subjects. Reveal offers additional diagnostic yield in complex elderly subjects with suspected cardiovascular causes of syncope or unexplained falls which have not been previously satisfactorily diagnosed despite extensive investigations.

Muscle fibre composition and electromyographic features of cervical muscles following prolonged head extension in growing rats.

Soft tissue stretching has been proposed as one of the control factors in craniofacial morphogenesis. However, its mechanism remains unclear. The present study investigated electromyographic (EMG) activity and muscle fibre composition of cervical muscles following prolonged head extension in growing rats. Thirty-six male Wistar rats were divided into two experimental (E1, E2) and one control (C) group at 25 days of age. To induce head extension, the experimental rats were raised in cylindrical cages, which were positioned horizontally for group E1 and tilted upward at 45 degrees for group E2. At 55 days of age, EMG activity was recorded from the anterior digastricus (AD), sternohyoideus (SH), sternomastoideus (SM), longus capitis (LC), and biventer cervicis (BC) muscles in the rest position and passive head extension. EMG activity was analysed on its integrated values (IEMG), and composition of muscle fibres was evaluated by myosin ATPase reaction and fibre cross-sectional areas were calculated. Group E1 showed a higher percentage of type I fibres and lower IEMG during passive head extension in AD. In group E2 there was a higher percentage of type I fibres, a higher IEMG at rest, and a lower IEMG during passive head extension in BC. The experimental groups demonstrated altered proportions of type IIA and IIB fibres in SM and LC. They also showed higher percentages of subtype fibres and reduced cross-section areas of type II fibres in most of the muscles investigated. These findings suggest that head extension affects fibre transition, distribution, cross-section area, and recruitment pattern in cervical muscles.

Factors Affecting Recovery After Acoustic Neuroma Resection

In order to determine which variables influence recovery from acoustic neuroma resection, acutely postoperative patients were divided into two groups and treated twice daily at bedside as inpatients at a tertiary care center. Treatment times were increased gradually from 5 to 30 min. Exercise subjects underwent passive and active head movements and walking with augmented head movements. Control subjects received attention without exercise. Pre- and post-tests included vertigo intensity and frequency, low-frequency vestibulo-ocular reflex (VOR), posturography and path integration. Post-tests were given at discharge and at &#44 4-week intervals for 3 months. Multilevel statistical analyses showed that neither group assignment nor age affected the outcome. All measures were abnormal at discharge but improved towards normal within 3 weeks. VOR on the unoperated side returned to normal values but on the lesioned side did not. Therefore, compensation is influenced by tumor size but not by age or early postoperative vestibular rehabilitation. Most compensation occurs within 3 weeks, probably due to central mechanisms, although some measures may not recover completely.

Vestibular convergence patterns in vestibular nuclei neurons of alert primates.

Sensory signal convergence is a fundamental and important aspect of brain function. Such convergence may often involve complex multidimensional interactions as those proposed for the processing of otolith and semicircular canal (SCC) information for the detection of translational head movements and the effective discrimination from physically congruent gravity signals. In the present study, we have examined the responses of primate rostral vestibular nuclei (VN) neurons that do not exhibit any eye movement-related activity using 0.5-Hz translational and three-dimensional (3D) rotational motion. Three distinct neural populations were identified. Approximately one-fourth of the cells exclusively encoded rotational movements (canal-only neurons) and were unresponsive to translation. The canal-only central neurons encoded head rotation in SCC coordinates, exhibited little orthogonal canal convergence, and were characterized with significantly higher sensitivities to rotation as compared to primary SCC afferents. Another fourth of the neurons modulated their firing rates during translation (otolith-only cells). During rotations, these neurons only responded when the axis of rotation was earth-horizontal and the head was changing orientation relative to gravity. The remaining one-half of VN neurons were sensitive to both rotations and translations (otolith + canal neurons). Unlike primary otolith afferents, however, central neurons often exhibited significant spatiotemporal (noncosine) tuning properties and a wide variety of response dynamics to translation. To characterize the pattern of SCC inputs to otolith + canal neurons, their rotational maximum sensitivity vectors were computed using exclusively responses during earth-vertical axis rotations (EVA). Maximum sensitivity vectors were distributed throughout the 3D space, suggesting strong convergence from multiple SCCs. These neurons were also tested with earth-horizontal axis rotations (EHA), which would activate both vertical canals and otolith organs. However, the recorded responses could not be predicted from a linear combination of EVA rotational and translational responses. In contrast, one-third of the neurons responded similarly during EVA and EHA rotations, although a significant response modulation was present during translation. Thus this subpopulation of otolith + canal cells, which included neurons with either high- or low-pass dynamics to translation, appear to selectively ignore the component of otolith-selective activation that is due to changes in the orientation of the head relative to gravity. Thus contrary to primary otolith afferents and otolith-only central neurons that respond equivalently to tilts relative to gravity and translational movements, approximately one-third of the otolith + canal cells seem to encode a true estimate of the translational component of the imposed passive head and body movement.

The transpiration cooled first wall and blanket concept

To achieve high thermal performance at high power density the EVOLVE concept was investigated under the APEX program. The EVOLVE W-alloy first wall and blanket concept proposes to use transpiration cooling of the first wall and boiling or vaporizing lithium (Li) in the blanket zone. Critical issues of this concept are: the Magnetohydrodynamic (MHD) pressure losses of the Li circuit, the evaporation through a capillary structure and the needed superheating of the Li at the first wall and blanket zones. Application of the transpiration concept to the blanket region results in the integrated transpiration cooling concept (ITCC) with either toroidal or poloidal first wall channels. For both orientations the routing of the liquid Li and the Li vapor has been modeled and the corresponding pressure losses have been calculated by varying the width of the supplying slot and the capillary diameter. The concept works when the sum of the active and passive pumping head is higher than the total system pressure losses and when the temperature at the inner side of the first wall does not override the superheating limit of the coolant. This cooling concept has been extended to the divertor design, and the removal of a surface heat flux of up to 10 MW/m 2 appears to be possible, but this paper will focus on the transpiration cooled first wall and blanket concept assessment.

Eighth-nerve regeneration, 20 years later

Over 20 years ago, Harold Zakon and Bob Capranica began a series of studies tracing the anatomical and physiological sequelae of damage to the eighth cranial nerve in ranid frogs. Their results indicated that the severed nerve could regenerate back into the brain, that proper anatomical connectivity was re-established, and that appropriate neural responses in target nuclei re-emerge. In an extension of these studies, patterns of gene expression in the crushed nerve and in target brainstem nuclei are being examined at various time points after damage. These molecular changes are correlated with the time course of recovery of normal vestibular function. Passive (head tilt) and active (response to rotation) vestibular function recover at different rates, with response to rotation still abnormal at 12 weeks after damage. This delayed recovery indicates a process of regeneration, rather than behavioral compensation. Differential display, a PCR-based technique, is used to elucidate which mRNAs are expressed at different time points following nerve crush. At periods less than 1 week after damage, mRNAs, both novel and previously identified, are differentially expressed in crushed versus sham-operated tissue. One gene product, expressed at 24 h post-crush, exhibits 91% coding region homology to human brain-specific protein, CGI-38.

Collicular microstimulation during passive rotation does not generate fixed gaze shifts.

We investigated whether saccades evoked by electrical stimulation (E-saccades) in the superior colliculus can compensate for passive sinusoidal head rotation in yaw so as to keep the rapid gaze shift constant. After accounting for variations in E-saccade onset position, we found significant horizontal metric changes, proportional to head velocity, in 31 of 37 experiments in 2 monkeys. Vertical effects were small. In a substantial fraction of the experiments (14/37), these metric changes represented significant but often insufficient compensatory adjustments in the horizontal component, opposite to the direction of head movement. However, very robust violations of gaze-shift constancy were remarkably common: significant anticompensatory changes in the horizontal component occurred in 17/37 experiments. In these cases, typically involving larger E-saccades, the horizontal component increased in size with rotation into the half field containing the E-saccade and became smaller during opposite rotation. Further analysis showed that, instead of showing a dichotomy, the metric effect actually varied along a continuum from compensatory to strongly anticompensatory. In addition to these metric changes, we found a robust kinematic effect of head rotation in metrically matched E-saccades. In all experiments where the effect was significant (34/37), horizontal peak velocity increased for rotation into the half field where the E-saccade was directed and decreased for opposite rotation. This kinematic effect was again proportional to head velocity and predominant in the horizontal component. Comparison of yaw and pitch rotation at the same stimulation site showed that both expressions of vestibular-saccade interaction (metric and kinematic) tended to align with the direction of rotation. The component-specific nature of the modulation suggests that the effects may have been caused by convergence of saccadic and vestibular signals at a component-coding stage downstream of the colliculus. We suggest that the quick-phase system got access to the common pulse generator as soon as the collicular stimulation had opened the pause-cell gate. Adding such an anticompensatory signal would act to increase the E-saccade horizontal component when the monkey was rotated in the same direction and bring about a decrease in size and peak velocity when it was opposite. In the large majority of experiments the metric changes failed to maintain gaze-shift constancy, either because they were in the wrong direction or because they were too small. Possible reasons for this major departure from the properties of natural gaze shifts are discussed.

Vestibuloocular reflex signal modulation during voluntary and passive head movements.

The vestibuloocular reflex (VOR) effectively stabilizes the visual world on the retina over the wide range of head movements generated during daily activities by producing an eye movement of equal and opposite amplitude to the motion of the head. Although an intact VOR is essential for stabilizing gaze during walking and running, it can be counterproductive during certain voluntary behaviors. For example, primates use rapid coordinated movements of the eyes and head (gaze shifts) to redirect the visual axis from one target of interest to another. During these self-generated head movements, a fully functional VOR would generate an eye-movement command in the direction opposite to that of the intended shift in gaze. Here, we have investigated how the VOR pathways process vestibular information across a wide range of behaviors in which head movements were either externally applied and/or self-generated and in which the gaze goal was systematically varied (i.e., stabilize vs. redirect). VOR interneurons [i.e., type I position-vestibular-pause (PVP) neurons] were characterized during head-restrained passive whole-body rotation, passive head-on-body rotation, active eye-head gaze shifts, active eye-head gaze pursuit, self-generated whole-body motion, and active head-on-body motion made while the monkey was passively rotated. We found that regardless of the stimulation condition, type I PVP neuron responses to head motion were comparable whenever the monkey stabilized its gaze. In contrast, whenever the monkey redirected its gaze, type I PVP neurons were significantly less responsive to head velocity. We also performed a comparable analysis of type II PVP neurons, which are likely to contribute indirectly to the VOR, and found that they generally behaved in a quantitatively similar manner. Thus our findings support the hypothesis that the activity of the VOR pathways is reduced "on-line" whenever the current behavioral goal is to redirect gaze. By characterizing neuronal responses during a variety of experimental conditions, we were also able to determine which inputs contribute to the differential processing of head-velocity information by PVP neurons. We show that neither neck proprioceptive inputs, an efference copy of neck motor commands nor the monkey's knowledge of its self-motion influence the activity of PVP neurons per se. Rather we propose that efference copies of oculomotor/gaze commands are responsible for the behaviorally dependent modulation of PVP neurons (and by extension for modulation of the status of the VOR) during gaze redirection.

Autonomic dysfunction and hemodynamics in vitamin B 12 deficiency

Orthostatic hypotension in patients with cobalamin (Cbl) deficiency has been reported previously in isolated cases but we are not aware of detailed systematic studies of hemodynamic and autonomic nervous system function in patients with cobalamin deficiency. We investigated hemodynamic and autonomic responses to 60° passive head up tilt (HUT) in 21 patients with vitamin B 12 deficiency, 21 healthy age-matched control subjects and 9 age-matched patients with diabetes mellitus (DM) and established diabetic neuropathy. To systematically assess hemodynamic and autonomic nervous system function, we performed measurements of heart rate, beat-to-beat systolic and diastolic blood pressure, stroke index, cardiac index, total peripheral resistance index, total power, low (LF) and high (HF) frequency oscillatory component of heart rate variability, LF/HF ratio and spontaneous baroreflex sensitivity. As compared to controls, we found a significant fall of systolic blood pressure during 60 consecutive beats directly after head up tilt; furthermore, a significantly blunted fall of stroke index, cardiac index and a lack of increase of total peripheral resistance index for the duration of tilt in patients with diabetes mellitus and in patients with vitamin B 12 deficiency. As compared to controls, we observed an altered response of spectral indices of sympathetic activation and vagal withdrawal and an impaired modulation of baroreflex sensitivity during head up tilt suggestive of a complex modification in the neural control activities in patients with cobalamin deficiency, which was comparable to that observed in patients with diabetes mellitus and established autonomic neuropathy. The results suggest that vitamin B 12 deficiency causes autonomic dysfunction with similar hemodynamic consequences and patterns of autonomic failure as seen in diabetic autonomic neuropathy. Defective sympathetic activation may be the cause for orthostatic hypotension, which is occasionally seen in patients with vitamin B 12 deficiency. It is concluded that patients with orthostatic hypotension should be screened for cobalamin deficiency.

CHRONOTROPIC INCOMPETENCE AND AUTONOMIC DYSFUCTION IN INDIVIDUALS WITH DOWN SYNDROME

Maximal heart rate (HR) during exercise is reduced in individuals with Down syndrome (DS). Most individuals with DS exhibit chronotropic incompetence and this may be a function of impaired autonomic control within this population. PURPOSE: We investigated HR changes during exercise and autonomic function in 20 individuals with DS (age = 25.1 yrs) and in 18 similarly aged control subjects (age = 28.4yrs). METHODS: All subjects completed a maximal treadmill test with heart rate and oxygen uptake measurements. On a separate day, autonomic function was evaluated using a 2-minute handgrip test at 30% of maximal voluntary contraction and a passive head up tilt protocol (80°). Beat-to-beat HR was measured throughout each test. RESULTS: Persons with DS had lower maximal HR (159 vs 188 bpm; p < .05), reduced heart rate reserve (88 vs 125 bpm;p < .05), a smaller increase in HR during the hand grip (8 vs 15 bpm;p < .05) and head up tilt tests (8 vs 14 bpm;p < .05). However, the relative increase in HR as a percent of HRR did not differ between groups during hand grip (8.4 vs 12%) or head up tilt testing (9.4 vs 11.8%). CONCLUSION: Persons with DS exhibit reduced HR responses to maximal exercise and to both sympathetic (hand grip) and orthostatic (head up tilt) challenges. However, the HR changes during hand grip and head up tilt testing was similar in both groups when expressed relative to HRR. Our data suggest that autonomic dysfunction contributes to the low maximal HR observed in individuals with DS. Thus, autonomic dysfunction may also contribute to the low aerobic capacity typically observed in persons with DS, since maximal HR is related to aerobic capacity in this population.

Factors Affecting Recovery After Acoustic Neuroma Resection

In order to determine which variables influence recovery from acoustic neuroma resection, acutely postoperative patients were divided into two groups and treated twice daily at bedside as inpatients at a tertiary care center. Treatment times were increased gradually from 5 to 30 min. Exercise subjects underwent passive and active head movements and walking with augmented head movements. Control subjects received attention without exercise. Pre- and post-tests included vertigo intensity and frequency, low-frequency vestibulo-ocular reflex (VOR), posturography and path integration. Post-tests were given at discharge and at , 4-week intervals for 3 months. Multilevel statistical analyses showed that neither group assignment nor age affected the outcome. All measures were abnormal at discharge but improved towards normal within 3 weeks. VOR on the unoperated side returned to normal values but on the lesioned side did not. Therefore, compensation is influenced by tumor size but not by age or early postoperative vestibular rehabilitation. Most compensation occurs within 3 weeks, probably due to central mechanisms, although some measures may not recover completely.

Oculomotor responses to active head movements in darkness: formulation and testing of a mathematical model.

Passive head rotation in darkness produces vestibular nystagmus, consisting of slow and quick phases. The vestibulo-ocular reflex produces the slow phases, and the saccadic mechanism produces the fast phases. A similar pattern of eye movements can be evoked by active head rotations in darkness, suggesting that vestibular nystagmus represents a specific strategy of eye-head coordination during natural behavior. We have investigated the way in which the saccadic components (quick phases) of such a response are generated and hypothesize a vestibulosaccadic pathway that conveys information on head rotation from the vestibular system to the saccade-generating mechanism in the brain stem.1–3 We recorded the eye and head movements of nine normal subjects elicited by active head rotations in darkness. Subjects were instructed to rotate their heads in a sinusoidal-like manner and to focus their attention on producing a smooth head rotation. Eye movements were quantitatively analyzed, and statistical analysis was performed in order to correlate the final eye position reached at the end of each saccade and the characteristics of the head movement, as velocity or acceleration. We found that a linear combination of head velocity and head displacement information provides the reference signal to the saccadic mechanism through the vestibulosaccadic pathway (correlation coefficient r2 range, 0.83–0.95). FIGURE 1 presents an example of an eye movement evoked by an active head rotation in darkness and of the reference signal to the saccadic mechanism. The reference signal was computed as a linear combination of head velocity and head displacement based on the following equation:

Signal processing by vestibular nuclei neurons is dependent on the current behavioral goal.

The vestibular sensory apparatus and associated vestibular nuclei are generally thought to encode angular head velocity during our daily activities. However, in addition to direct inputs from vestibular afferents, the vestibular nuclei receive substantial projections from cortical, cerebellar, and other brainstem structures. Given this diversity of inputs, the question arises: How are the responses of vestibular nuclei neurons to head velocity modified by these additional inputs during naturally occurring behaviors? Here we have focused on the signal processing done by two specific classes of neurons in the vestibular nuclei: (1) position-vestibular-pause (PVP) neurons that mediate the vestibulo-ocular reflex (VOR), and (2) vestibular-only (VO) neurons that are thought to mediate, at least in part, the vestibulo-collic reflex (VCR). We first characterized neuronal responses to passive rotation in the head-restrained condition, and then released the head to record the discharges of the same neurons during self-generated head movements. VOR interneurons (i.e., PVP neurons) faithfully transmitted head velocity signals when the animal stabilized its gaze, regardless of whether the head motion was actively or passively generated; their responses were attenuated only when the monkey's behavioral goal was to redirect its axis of gaze relative to space. In contrast, VCR interneurons (i.e., VO neurons) faithfully transmitted head velocity signals during passive head motion, but their responses were greatly (and similarly) attenuated during all behaviors (i.e., gaze shifts, gaze pursuit, gaze stabilization) during which the monkey's behavioral goal was to move its head relative to the body. To characterize the mechanism(s) that underlie this differential processing, we tested neurons during passive rotation of the head relative to the body, as well as during a task in which a monkey actively "drove" both its head and body together in space. We conclude that neither passive activation of neck proprioceptors nor knowledge of self-generated head-in-space motion directly mediate the observed reductions in head-velocity-related modulation. Instead, we propose that the VOR and VCR pathways use efference copies of oculomotor and neck movement commands, respectively, for the differential processing of vestibular information.

Head unrestrained horizontal gaze shifts after unilateral labyrinthectomy in the rhesus monkey.

Following the orienting saccade of a combined eye-head gaze shift, normal monkeys exhibit a compensatory eye counterrotation that stabilizes gaze as the head movement continues. This counterrotation, which has a gain (eye velocity/head velocity) of near unity, is a manifestation of the vestibulo-ocular reflex (VOR). Acute unilateral labyrinthectomy (UL) causes severe asymmetry in the VOR during passive head rotations that recovers incompletely over time. The purpose of this investigation was to compare the recovery of the counterrotation gain during horizontal gaze shifts with that of the passive VOR after UL. During the 1st week after UL, counterrotation gains were asymmetric, being lower for head movements towards the lesion but nearly normal for head movements towards the intact side. Whereas this asymmetry in the counterrotation gain resolved within a week after UL, asymmetries in the passive VOR persisted. During the 1st week after UL, behavioral performance was generally poor, with a high incidence of inaccurate gaze shifts and larger latencies. In addition, animals used slower head movements such that peak head amplitude during the eye saccade was significantly lower during the 1st week after UL as compared to control values. Bilateral labyrinthectomy (BL) resulted in larger but symmetric deficits in counterrotation, which, contrary to the passive VOR, exhibited significant recovery over time. It is hypothesized that recovery of counterrotation gain after UL has contributions from multiple sources, including the contralateral intact labyrinth and an efference copy of the head movement.

Selective Processing of Vestibular Reafference during Self-Generated Head Motion

The vestibular sensory apparatus and associated vestibular nuclei are generally thought to encode head-in-space motion. Angular head-in-space velocity is detected by vestibular hair cells that are located within the semicircular canals of the inner ear. In turn, the afferent fibers of the vestibular nerve project to neurons in the vestibular nuclei, which, in head-restrained animals, similarly encode head-in-space velocity during passive whole-body rotation. However, during the active head-on-body movements made to generate orienting gaze shifts, neurons in the vestibular nuclei do not reliably encode head-in-space motion. The mechanism that underlies this differential processing of vestibular information is not known. To address this issue, we studied vestibular nuclei neural responses during passive head rotations and during a variety of tasks in which alert rhesus monkeys voluntarily moved their heads relative to space. Neurons similarly encoded head-in-space velocity during passive rotations of the head relative to the body and during passive rotations of the head and body together in space. During all movements that were generated by activation of the neck musculature (voluntary head-on-body movements), neurons were poorly modulated. In contrast, during a task in which each monkey actively "drove" its head and body together in space by rotating a steering wheel with its arm, neurons reliably encoded head-in-space motion. Our results suggest that, during active head-on-body motion, an efferent copy of the neck motor command, rather than the monkey's knowledge of its self-generated head-in-space motion or neck proprioceptive information, gates the differential processing of vestibular information at the level of the vestibular nuclei.

Role of the cerebellar flocculus region in cancellation of the VOR during passive whole body rotation.

A series of studies were carried out to investigate the role of the cerebellar flocculus and ventral paraflocculus in the ability to voluntarily cancel the vestibuloocular reflex (VOR). Squirrel monkeys were trained to pursue moving visual targets and to fixate a head stationary or earth stationary target during passive whole body rotation (WBR). The firing behavior of 187 horizontal eye movement-related Purkinje (Pk) cells in the flocculus region was recorded during smooth pursuit eye movements and during WBR. Half of the Pk cells encountered were eye velocity Pk cells whose firing rates were related to eye movements during smooth pursuit and WBR. Their sensitivity to eye velocity during WBR was reduced when a visual target was not present, and their response to unpredictable steps in WBR was delayed by 80-100 ms, which suggests that eye movement sensitivity depended on visual feedback. They were insensitive to WBR when the VOR was canceled. The other half of the Purkinje cells encountered were sensitive to eye velocity during pursuit and to head velocity during VOR cancellation. They resembled the gaze velocity Pk cells previously described in rhesus monkeys. The head velocity signal tended to be less than half as large as the eye velocity-related signal and was observable at a short ( approximately 40 ms) latency when the head was unpredictably accelerated during ongoing VOR cancellation. Gaze and eye velocity type Pk cells were found to be intermixed throughout the ventral paraflocculus and flocculus. Most gaze velocity Pk cells (76%) were sensitive to ipsilateral eye and head velocity, but nearly half (48%) of the eye velocity Pk cells were sensitive to contralateral eye velocity. Thus the output of flocculus region is modified in two ways during cancellation of the VOR. Signals related to both ipsilateral and contralateral eye velocity are removed, and in approximately half of the cells a relatively weak head velocity signal is added. Unilateral injections of muscimol into the flocculus region had little effect on the gain of the VOR evoked either in the presence or absence of visual targets. However, ocular pursuit velocity and the ability to suppress the VOR by fixating a head stationary target were reduced by approximately 50%. These observations suggest that the flocculus region is an essential part of the neural substrate for both visual feedback-dependent and nonvisual mechanisms for canceling the VOR during passive head movements.

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.

Vestibular compensation and substitution.

This is a very brief update on the major papers since August 1998. Unilateral vestibular loss causes oculomotor, postural and sensory symptoms, all of which would be appropriate responses in a healthy person to a strong maintained angular and linear acceleration stimulus directed towards the healthy side. Within hours or days these static symptoms (so called because they are present without any externally imposed vestibular stimulation) reduce, and their progressive disappearance is called 'vestibular compensation'. However, careful testing with natural vestibular stimuli shows that the dynamic vestibular response after unilateral vestibular loss to passively imposed vestibular stimuli does not recover; it is usually asymmetric and functionally ineffective. Major recent developments are: (1) the permanent asymmetrical and functionally ineffective dynamic rotational vestibulo-ocular reflex responses to passive natural vestibular stimulation after unilateral vestibular loss and canal blocks in human patients; (2) evidence for the substitution of other sensory input and responses during vestibular compensation; (3) perceptual testing using visual perception of a horizontal line to confirm permanent otolith dysfunction; (4) the clear and substantial differences in post-unilateral vestibular loss vestibulo-ocular reflex responses between passive and active head turning; and (5) new results in brainstem physiology explaining the disappearance of static symptoms.

Investigation of Trunk and Extremity Movement Associated With Passive Head Turning in Newborns

Physical therapist examination of pediatric clients or clients with neurological conditions often includes the observation of stereotypical movement patterns such as the asymmetrical tonic neck reflex and righting reactions. The purpose of this study was to investigate whether extremity and trunk responses to passive head turning could be documented in newborn infants. Forty-two newborns with no known medical problems were videotaped within 5 days of birth while an investigator turned their heads left and right. Videotapes were stopped at 5-second intervals to record the direction of head turn with the rest of the body obscured. A second investigator recorded trunk and extremity position with the head obscured. The direction of head turning affected upper- and lower-extremity position, with extension stronger on the face side. The direction of trunk convexity was also affected by head position, with the trunk convex to the side to which the face was turned. Extremity responses and trunk responses to passive head turning can be documented corresponding to patterns reported for the asymmetrical tonic neck reflex and righting reflexes in neonates with no known medical problems more frequently than would occur by chance.