Rostral Fastigial Nucleus Activity in the Alert Monkey During Three-Dimensional Passive Head Movements

We recorded three-dimensional eye and head movements during circular, horizontal, vertical, and torsional head shaking in six human subjects with normal vestibular function. With circular head shaking, the stimulation of the canals by the termination of the head movement is similar to that following a step in velocity about the naso-occipital axis. A large torsional nystagmus with slow phase eye velocity of about 20 degrees/s was observed upon cessation of circular head shaking. The three-dimensional eye movements expected from stimulation of the semicircular canals by the head-shaking maneuvers were calculated. The predicted activation of the canals was determined by projecting the head velocity (in head coordinates) into the canal planes and then processing the signal with the transfer function of the canals. The torsional eye velocity components predicted by the stimulation of the canals matched the recorded ones. We observed small horizontal eye velocities that could not be predicted by the stimulation of the canals alone. No eye movements were observed after the end of head shaking about a fixed horizontal or vertical axis. The eye velocities following the termination of head oscillations in the roll plane were small. The analysis methods developed for this study may be useful in the investigation of eye movements elicited by other types of three-dimensional head movements.

1. To study their contribution to the vestibulocollic reflex, we have studied, in decerebrate paralyzed cats, the effect of sinusoidal vestibular stimulation in multiple vertical planes on the spontaneous activity of neurons in the C3 ventral horn. Antidromic microstimulation was used to identify 17/42 neurons as commissural; 10 of these were confirmed to have a projection to the contralateral ventral horn. 2. Dynamics of the responses of spontaneously firing neurons were studied with 0.05-1 Hz sinusoidal stimuli delivered near the plane of rotation that produced maximal modulation of neuron activity (response vector orientation). On the basis of their responses, we classified 38 neurons as receiving otolith, semicircular canal, or otolith + canal input. All three response types were found among commissure and nonantidromic neurons. 3. Two-thirds of neuron response vector orientations pointed contralaterally. They were either near the anterior or posterior canal planes or in the roll quadrant. In the case of neurons with input from canals, the latter indicates convergence from the vertical canals on the same side. There were almost no vectors in the pitch quadrants. The distribution of response vector orientations resembles that seen in the vestibular nuclei and pontomedullary reticular formation, suggesting that commissural neurons may not make a new contribution to spatial processing in the vertical vestibulocollic reflex. 4. It is presumed that commissural neurons are premotor. If so, some have the properties to be in the pathway between the contralateral utricle and neck motoneurons. More generally, their actions could modify the effectiveness of vestibulospinal and reticulospinal fibers that have similar spatial properties and make synapses with neck motoneurons.

The contribution of the fastigial nucleus and the vestibular nerves (eighth cranial nerves) to the orthostatic reflexes in anesthetized, paralyzed cats was studied. Bilateral lesions of the rostral fastigial nucleus resulted in impairment of the reflex changes in blood pressure, femoral arterial flow, and resistance evoked by head-up tilting to 30° or 60°. The deficit consisted of an increase in the magnitude of the initial fall in blood pressure during tilting. The effects on blood pressure were paralleled by decreased vasoconstriction in the femoral artery. Extracranial lesions of the vestibular nerves produced comparable deficits which were not enhanced by subsequent lesions of the fastigial nucleus. Denervation of the baroreceptors impaired the reflexes, and subsequent lesion of the fastigial nucleus increased this deficit. The pressor response evoked by electrical stimulation of the rostral fastigial nucleus also reversed the deficit in orthostasis produced by hemorrhage. Small doses of sodium pentobarbital which did not alter the resting blood pressure or the pressor response to carotid occlusion impaired the responses to stimulation of the fastigial nucleus and tilting. Therefore, the rostral fastigial nucleus, which might be triggered by the vestibular apparatus, appears to participate in concert with the baroreceptors in the initiation and possibly the maintenance of the orthostatic reflexes.

To locate the cerebellar-activated descending sympathetic pathways in the dog the fastigial nucleus (FN) was electrically stimulated in chloralose-anesthetized dogs while recording from sympathetic preganglionic neurons. Physiological interventions included lesions in the dorsolateral funiculus (DLF) of the spinal cord, myelotomy, arterial pressure changes, bilateral occlusion of the carotid arteries, and administration of clonidine. Multiunit activity at the T2 on T3 white ramus communicans was recorded on-line during rest and FN stimulation. Descending sympathetic activity (averaging 3.5 m/s) in the DLF was increased in response to FN stimulation but was significantly reduced by ipsilateral and eliminated by bilateral FN lesions. When testing for the effects of baroreceptor reflexes on the sympathetic pathway phenylephrine-induced hypertension decreased, but moderate hemorrhage increased the amount of preganglionic activity at rest and during FN stimulation. During hypertension and simultaneous carotid artery occlusion the amount of sympathetic activity that could be evoked was comparable to that evoked during normotensive states. Clonidine (IV) reduced the FN sympathoexcitation, but direct stimulation of the DLF indicated that clonidine had sympathoinhibitory activity at both medullary and spinal sites. In summary, rostral FN primarily excited ipsilateral descending sympathetic pathways in DLF, and this sympathoexcitation was partially inhibited by baroreceptor intervention.

Single-unit recordings were obtained from central vestibular neurons in three monkeys during passive head movements. Neurons that discharged in relation to head translation or changes in head orientation, but not eye movement ("vestibular-only," n = 154), were examined in detail. Neuronal discharge rates were analyzed during four stimulus conditions: sinusoidal head translation in the horizontal plane (0.2-4 Hz, 0.2 g peak acceleration), static head tilt in the vertical plane (+/-20 degrees ), oscillatory head tilt (0.5-2 Hz), and sinusoidal angular rotation about an earth-vertical axis (0.5 or 1 Hz). Vestibular-only cells were divided into two groups based on the regularity of their spontaneous discharge rates (CV*). One group (low-sensitivity units) exhibited regular discharge rates (CV* < 0.2), weak discharge modulation during head translation (<25 spikes . s(-1) . g(-1) at f = 1 Hz), and persistent discharge rates related to static head tilt (0.68 spikes . s(-1) . degrees (-1) of head tilt). The second group (high sensitivity neurons) exhibited irregular discharge rates (CV* > 0.2), strong discharge modulation during head translation ( approximately 100 spikes . s(-1) . g(-1) at f = 1 Hz), and little or no change in discharge rate during static head tilt (0.32 spikes . s(-1) . degrees (-1)). The firing rates of some neurons in both groups were modulated during rotation about an earth-vertical axis (42%), but the modulation was greater for neurons classified as high sensitivity units. Previous reports have described neurons similar to the high sensitivity group; however, the low sensitivity or tilt neurons have not previously been characterized. Significantly, recent theoretical models have predicted neurons with discharge patterns similar to those of low- and high-sensitivity neurons.

Premotor circuits driving extraocular motoneurons and downstream motor outputs of cerebellar nuclei are well known. However, there is, as yet, no unequivocal account of cerebellar output pathways controlling eye movements in primates. Using retrograde transneuronal transfer of rabies virus from the lateral rectus (LR) eye muscle, we studied polysynaptic pathways to LR motoneurons in primates. Injections were placed either into the central or distal muscle portion, to identify innervation differences of LR motoneurons supplying singly innervated (SIFs) or multiply innervated muscle fibers (MIFs). We found that SIF motoneurons receive major cerebellar 'output channels' bilaterally, while oligosynaptic cerebellar innervation of MIF motoneurons is negligible and/or more indirect. Inputs originate from the fastigial nuclei di- and trisynaptically, and from a circumscribed rostral portion of the ventrolateral interpositus posterior and from the caudal pole of the dentate nuclei trisynaptically. While disynaptic cerebellar inputs to LR motoneurons stem exclusively from the caudal fastigial region involved in saccades, pursuit and convergence (via its projections to brainstem oculomotor populations), minor trisynaptic inputs from the rostral fastigial nucleus, which contributes to gaze shifts, may reflect access to vestibular and reticular eye-head control pathways. Trisynaptic inputs to LR motoneurons from the rostral ventrolateral interpositus posterior, involved in divergence (far-response), is likely mediated by projections to the supraoculomotor area, contributing to LR motoneuron activation during divergence. Trisynaptic inputs to LR motoneurons from the caudal dentate, which also innervates disynaptically the frontal and parietal eye fields, can be explained by its superior colliculus projections, and likely target saccade-related burst neurons.

Although substantial research demonstrates that intervertebral disc cells respond to mechanical signals, little research has been done to characterize the in vivo mechanical environment in the disc tissue. The objective of this study was to estimate cervical disc strain during three-dimensional head movements. Twenty-nine young healthy adults performed full range of motion flexion/extension, lateral bending, and axial rotation of the head within a biplane radiography system. Three-dimensional vertebral kinematics were determined using a validated model-based tracking technique. A computational model used these kinematics to estimate subject-specific intervertebral disc deformation (C3-4 to C6-7). Peak compression, distraction and shear strains were calculated for each movement, disc level, and disc region. Peak compression strain and peak shear strain were highest during flexion/extension (mean ± 95% confidence interval) (32 ± 3 and 86 ± 8%, respectively), while peak distraction strain was highest during lateral bending (57 ± 5%). Peak compression strain occurred at C4-5 (33 ± 4%), while peak distraction and shear strain occurred at C3-4 (54 ± 8 and 83 ± 11%, respectively). Peak compression, distraction, and shear strains all occurred in the posterior-lateral annulus (48 ± 4, 80 ± 8, and 109 ± 12%, respectively). These peak strain values may serve as boundary conditions for in vitro loading paradigms that aim to assess the biologic response to physiologic disc deformations.

Neural Activity Pattern in Different Brain Stem Structures during Eye-Head Movements

The temporal processing in the encoding of head rotation was investigated by comparing the dynamics of vestibular nuclei neurons with those of the regularly and irregularly firing semicircular canal afferents in alert rhesus monkeys. During earth-vertical axis rotations, neurons without eye movement sensitivity differed in their response dynamics from both regularly and irregularly firing semicircular canal afferents. At high frequencies, central responses increased in sensitivity and maintained phase leads of nearly 30 degrees relative to head velocity. These persistent high-frequency phase leads resembled those of irregularly firing (but not regularly firing) semicircular canal afferents. However, at low frequencies, central responses exhibited significantly smaller phase leads than those of irregularly firing semicircular canal afferents, and dynamics resembled more those of the regularly firing afferents. The response dynamics of central non-eye movement cells were significantly different from those of position-vestibular-pause and eye-head neurons (collectively referred to as eye movement cells). In contrast to the persistent phase leads of non-eye movement neurons, all eye movement cells modulated closely in phase with head velocity at all frequencies down to 0.05 Hz during visual suppression tasks. Vertical canal non-eye movement neurons that were insensitive to both translations and static head tilts led head velocity by approximately 5-30 degrees during high-frequency earth-horizontal axis rotations. Unlike the earth-vertical axis responses that led head velocity at low frequencies by as much as 20-40 degrees, vertical canal neurons only slightly led or even lagged behind head velocity during low-frequency earth-horizontal axis rotations. Posterior canal central non-eye movement cells lagged behind head velocity significantly more than anterior canal neurons. These frequency dependencies of central vestibular neurons in comparison with those of the afferents suggest that both low- and high-pass filtering might be necessary to convert primary semicircular canal afferent response dynamics to central neuron ones.

Cervical spine manipulation alters sensorimotor integration: A somatosensory evoked potential study

Spatiotemporal response properties of cerebellar Purkinje cells to animal displacement: a population analysis

Previous studies reported that balance deficits in pitch (sagittal) and roll (lateral) planes during stance and gait after onset of an acute unilateral peripheral vestibular deficit (aUPVD) due to vestibular neuritis are weakly correlated with deficits in commonly explored lateral canal vestibular ocular reflex (VOR) responses. Theoretically, stronger correlations with roll and pitch balance deficits could be expected for vertical canal VOR responses. Therefore, we investigated these correlations. University Hospital. Retrospective case review. Thirty three patients examined on average 5 days following onset of aUPVD. Video head impulse test (vHIT) VOR gains in each vertical canal plane were converted to roll and pitch response asymmetries and correlated with patients' roll and pitch balance control measured during stance and gait with body-worn gyroscopes mounted at lumbar 1 to 3. Mean caloric canal paresis was 92 ± 12%. Deficit side lateral vHIT mean gain was 0.4 ± 0.12, anterior gain 0.44 ± 0.18, and posterior gain, greater, 0.69 ± 0.15. Lateral VOR response gain asymmetries (37.2 ± 11.0%) were greater than roll VOR asymmetries calculated from all four vertical canal vHIT gains (16.2 ± 10.2%, p < 0.0001) and correlated (R = 0.56, p = 0.002). Pitch gain VOR asymmetries were less (4.9 ± 9.9%, p < 0.0001). All gait, but no stance, trunk roll angular velocity measures were correlated (p ≤ 0.03) with VOR roll asymmetries. This report links roll balance control deficits during gait with roll VOR deficits and emphasises the need to perform anterior canal vHIT to judge effects of an aUPVD on balance control. Pitch VOR asymmetries were weakly affected by vestibular neuritis.

1. Changes in regional blood flow and cardiodynamics were measured in anaesthetized paralysed cats during electrical stimulation of the rostral fastigial nucleus.2. Fastigial stimulation results in a graded, highly reproducible and stereotyped cardiovascular response characterized by (a) increased systolic, diastolic and mean arterial pressures without changes in central venous or occluded vein pressure, (b) decreased blood flow and increased vascular resistance in the axillary, renal, femoral and mesenteric arteries, increased flow without any change in vascular resistance in the common carotid artery, and increase in total peripheral resistance, (c) a small increase in heart rate and myocardial contractile force, decrease in calculated stroke volume, and no change in the cardiac output.3. Changes in regional arterial flow were abolished by transection of sympathetic nerves or blockade of alpha-adrenergic receptors by systemic administration of phentolamine.4. Changes in heart rate and myocardial contractility were abolished by stellate ganglionectomy or blockade of beta-adrenergic receptors by propranolol.5. No changes in pupillary diameter or retraction of the nictitating membrane were seen during fastigial stimulation with stimuli producing substantial changes in blood pressure.6. The fastigial pressor response represents a highly reproducible, stereotyped, graded, and differentiated pattern of activation of sympathetic preganglionic neurones.7. The pattern of cardiovascular effects of fastigial stimulation simulates the compensatory (orthostatic) reflex response to maintenance of an upright posture.8. Fastigial stimulation appears to excite the neural network subserving orthostatic reflexes.

IntroductionWhile most head movements in daily life are active, most tools used to assess vestibular deficits rely on passive head movements. A single gain value is not sufficient to quantify gaze stabilization efficiency during active movements in vestibular deficit patients. Moreover, during active gaze shifts, anticipatory mechanisms come into play. Our aim was to explore the extent to which previously described compensatory mechanisms are employed in patients with bilateral vestibular loss.MethodsWe used a Video Head Impulse Test (vHIT) to simultaneously record eye and head movements during a video Active Gaze Shift Test (vAGST). Thirty-eight patients with bilateral vestibular deficits and 61 control subjects were tested.ResultsDespite impaired performance on caloric tests and vHIT, most patients exhibited normal gaze stabilization (gain = 0.92 ± 0.1) during active gaze shifts up to a head speed (‘stall speed’) of approximately 140 ± 60°/sec, compared to 280 ± 65°/sec in controls. Our results indicate that BVD patients spontaneously adopt a head speed during active horizontal movements that significantly improves gaze stabilization compared to passive movements. The stall speed correlates with the spontaneous head speed typically adopted by BVD patients and controls in daily activities. As a consequence of the reduction in head speed and corrective saccades, patients also showed an increased delay in gaze stabilization (413 ± 105 ms in BVD patients versus 358 ± 82 ms in controls) at the end of the gaze shift, which might become disabling for certain tasks.DiscussionRecent model suggests that compensatory eye movements, which stabilize gaze during the counter rotation phase of active gaze shifts, are predictive in nature. vAGST is not designed to provide an etiological diagnosis but rather a functional assessment of the patient’s ability to generate predictive eye movements that compensate for vestibular sensor deficits. Understanding the quality of the patient’s sensory predictions can also shed light on vestibular symptoms, even in cases where no vestibular sensor deficit is detected. This suggest that quality of life and oscillopsia questionnaires should distinguish between predictable and unpredictable movements.

The vestibulo-ocular and vestibulo-spinal network provides the ability to hold gaze fixed on an object during passive head movement. Within that network, most of the second-order neurons of the medial vestibular nucleus (MVNn) compute internal representations of head movement velocity in the horizontal plane. Our previous in vitro studies of the MVNn membrane properties indicated that they may play a major role in determining the dynamic properties of these neurons independently of their connectivity. The present study investigated that hypothesis at a theoretical level. Biophysical models of type A and B MVNn were developed. Two factors were found to be important in modeling tonic and phasic firing activity: the activation of the delayed potassium current and the rate of calcium flux. In addition, the model showed that the strength of the delayed potassium current may determine the different forms of action potentials observed experimentally. These two models (type A and B cells) were examined using depolarizing stimulation, random noise, step, ramp and sinusoidal inputs. For random noise, type A cells showed stable (regular) firing frequencies, while type B cells exhibited irregular activity. With step stimulation, the models exhibited tonic and phasic firing responses, respectively. Using ramp stimulations, frequency versus current curves showed a linear response for the type B neuron model. Finally, with sinusoidal stimulation of increasing frequencies, the type A model demonstrated a decrease in sensitivity, while the type B model exhibited an increase in sensitivity. These theoretical results support the hypothesis that MVNn intrinsic membrane properties specify various types of dynamic properties amongst these cells and therefore contribute to the wide range of dynamic responses which characterize the vestibulo-ocular and vestibulo-spinal network.