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In order to ameliorate the consequences of ego motion for vision, human and nonhuman observers generate reflexive, compensatory eye movements based on visual as well as vestibular information, helping to stabilize the images of visual scenes on the retina despite ego motion. And in order to fully exploit the advantages of foveal vision, they make saccades to shift the image of an object onto the fovea and smooth pursuit eye movements to stabilize it there despite continuing object movement relative to the observer. With the exception of slow visually driven eye movements, which can be understood as manifestations of relatively straightforward feedback systems, most eye movements require a direct conversion of sensory input into appropriate motor responses in the absence of immediate sensory feedback. Hence, in order to generate appropriate oculomotor responses, the parameters linking input and output must be chosen suitably. Moreover, as the parameters may change from one manifestation of a movement to the next, for instance because of oculomotor fatigue, the choices should also be quickly modifiable. This chapter will present evidence showing that this fast parametric optimization, understood as a functionally distinct example of motor learning, is an accomplishment of specific parts of the cerebellum devoted to the control of eye movements. It will also discuss recent electrophysiological results suggesting how this specific form of motor learning may emerge from information processing in cerebellar circuits., (© 2014 Elsevier B.V. All rights reserved.)

Throughout Bernard Cohen's active career at Mount Sinai that lasted over a half century, he was involved in research on vestibular control of the oculomotor, body postural, and autonomic systems in animals and humans, contributing to our understanding of such maladies as motion sickness, mal de débarquement syndrome, and orthostatic syncope. This review is an attempt to trace and connect Cohen's varied research interests and his approaches to them. His influence was vast. His scientific contributions will continue to drive research directions for many years to come.

Throughout Bernard Cohen's active career at Mount Sinai that lasted over a half century, he was involved in research on vestibular control of the oculomotor, body postural, and autonomic systems in animals and humans, contributing to our understanding of such maladies as motion sickness, mal de débarquement syndrome, and orthostatic syncope. This review is an attempt to trace and connect Cohen's varied research interests and his approaches to them. His influence was vast. His scientific contributions will continue to drive research directions for many years to come. [ABSTRACT FROM AUTHOR]

Computational capability and connectivity are key elements for understanding how central vestibular neurons contribute to gaze-stabilizing eye movements during self-motion. In the well-characterized and segmentally distributed hindbrain oculomotor network of goldfish, we determined afferent and efferent connections along with discharge patterns of descending octaval nucleus (DO) neurons during different eye motions. Based on activity correlated with horizontal eye and head movements, DO neurons were categorized into two complementary groups that either increased discharge during both contraversive (type II) eye (e) and ipsiversive (type I) head (h) movements (eIhII) or vice versa (eIhII). Matching time courses of slow-phase eye velocity and corresponding firing rates during prolonged visual and head rotation suggested direct causality in generating extraocular motor commands. The axons of the dominant eIhII subgroup projected either ipsi- or contralaterally and terminated in the abducens nucleus, Area II, and Area I with additional recurrent collaterals of ipsilaterally projecting neurons within the parent nucleus. Distinct feedforward commissural pathways between bilateral DO neurons likely contribute to the generation of eye velocity signals in eIhII cells. The shared contribution of DO and Area II neurons to eye velocity storage likely represents an ancestral condition in goldfish that is clearly at variance with the task separation between mammalian medial vestibular and prepositus hypoglossi neurons. This difference in signal processing between fish and mammals might correlate with a larger repertoire of visuo-vestibular-driven eye movements in the latter species that potentially required a shift in sensitivity and connectivity within the hindbrain-cerebello-oculomotor network. NEW & NOTEWORTHY We describe the structure and function of neurons within the goldfish descending octaval nucleus. Our findings indicate that eye and head velocity signals are processed by vestibular and Area II velocity storage integrator circuitries whereas the velocity-to-position Area I neural integrator generates eye position solely. This ancestral condition differs from that of mammals, in which vestibular neurons generally lack eye position signals that are processed and stored within the nucleus prepositus hypoglossi. [ABSTRACT FROM AUTHOR]

Abstract:The objective of this study was to compare the findings of the bedside head impulse test (HIT), passive head rotation gain, and caloric irrigation in patients with cerebellar ataxia (CA). In 16 patients with CA and bilaterally pathological bedside HIT, VOR gains were measured during HIT and passive head rotation by scleral search coil technique. Eight of the patients had pathologically reduced caloric responsiveness, while the other eight had normal caloric responses. Those with normal calorics showed a slightly reduced HIT gain (mean±SD: 0.73±0.15). In those with pathological calorics, gains 80ms and 100 ms after the HIT as well as the passive rotation VOR gains were significantly lower. The corrective saccade after head turn occurred earlier in patients with pathological calorics (111±62 ms after onset of the HIT) than in those with normal calorics. (191±17 ms, p=0.0064) We indentified two groups of patients with CA: those with an isolated moderate HIT deficit only, probably due to floccular dysfunction, and those with combined HIT, passive rotation and caloric deficit, probably due to a peripheral vestibular deficit. From a clinical point of view, these results show that the bedside HIT alone can be false positive for establishing a diagnosis of a bilateral peripheral vestibular deficit in patients with CA.

The objective of this study was to compare the findings of the bedside head-impulse test (HIT), passive head rotation gain, and caloric irrigation in patients with cerebellar ataxia (CA). In 16 patients with CA and bilaterally pathological bedside HIT, vestibuloocular reflex (VOR) gains were measured during HIT and passive head rotation by scleral search coil technique. Eight of the patients had pathologically reduced caloric responsiveness, while the other eight had normal caloric responses.Those with normal calorics showed a slightly reduced HIT gain (mean±SD: 0.73±0.15). In those with pathological calorics, gains 80 and 100ms after the HIT as well as the passive rotation VOR gains were significantly lower. The corrective saccade after head turn occurred earlier in patients with pathological calorics (111±62ms after onset of the HIT) than in those with normal calorics (191±17 ms, p =0.0064).We identified two groups of patients with CA: those with an isolated moderate HIT deficit only, probably due to floccular dysfunction, and those with combined HIT, passive rotation, and caloric deficit, probably due to a peripheral vestibular deficit. From a clinical point of view, these results show that the bedside HIT alone can be false-positive for establishing a diagnosis of a bilateral peripheral vestibular deficit in patients with CA. [ABSTRACT FROM AUTHOR]

Vestibuloocular reflex (VOR) performance and adaptation have been investigated during antagonism of cerebellar AMPA/quisqualate and kainate receptors (AMPA/KA) by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). Injection of CNQX into the vestibulo-cerebellum of the goldfish before adaptation significantly inhibited and, at the highest dosage, completely prevented acquisition of adaptive reflex gain increases and decreases during a 3-h training period. Injection of CNQX before initiation of VOR adaptive training did not affect pre-adapted baseline performance of the reflex. Injection of CNQX, 1 to 2 h after the initiation of training did not alter the performance of adaptive gain increases that occurred before the injection. If injection of CNQX occurred at the end of adaptive training, there was an accelerated loss of the previously adapted gain changes during the retention period when the animal remained stationary in the dark. CNQX injection did not produce any permanent or long-term deficits, because goldfish could be retrained 48 h later to produce adaptive VOR gain changes similar to control animals. Thus, this work demonstrates that the AMPA/KA receptors located in the vestibulo-cerebellum of the goldfish are necessary for acquisition of short-term adaptive VOR gain increases and decreases. The deficit in adaptive capability was not the result of a deficit in performance, because CNQX did not inhibit an adaptive change that had already occurred as long as the adapting vestibular and visual stimulation continued. This adaptive performance could possibly be maintained by other glutamatergic (metabotropic) receptors located on the Purkinje cells. The retention of adapted gain increases and decreases after CNQX application was inhibited because AMPA/KA antagonism accelerated VOR gain loss after the completion of training when no vestibular or visual stimulation was present. Because the AMPA/KA receptors are located only in the molecular layer of the goldfish cerebellum, these results are, presumably, the result of AMPA/KA receptor antagonism at synapses located on the Purkinje cell dendrite tree. [ABSTRACT FROM AUTHOR]