Publications by authors named "Curthoys I"

The normal horizontal vestibulo-ocular reflex (HVOR) is largely generated by simultaneous stimulation of the two horizontal semicircular canals (HSCCs). To determine the dynamics of the HVOR when it is generated by only one HSCC, compensatory eye movements in response to a novel vestibular stimulus were measured using magnetic search coils. The vestibular stimulus consisted of low-amplitude, high-acceleration, passive, unpredictable, horizontal rotations of the head with respect to the trunk.

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One index of otolith function is the so-called oculogravic "illusion" that during centrifugal stimulation a small luminous bar, fixed with respect to the observer, appears to be roll-tilted by the same amount that the observer feels to be roll-tilted. Many patients undergoing therapeutic unilateral vestibular nerve section show the illusion symmetrically for left and right roll-tilts prior to the operation, but at testing one week after vestibular nerve section show a large asymmetry: they perceive the illusion when the resultant force is directed toward their intact ear, but they perceive a much reduced illusion when the force is directed toward their operated ear. This roll-tilt perceptual response asymmetry appears similar to the asymmetrical horizontal semicircular canal vestibulo-ocular responses for symmetrical but opposite head accelerations that these same patients exhibit for values of head angular accelerations in the natural range (Ewald's second law), and the present paper suggests that a version of Ewald's second law may apply to the otolithic system: specifically, that there is a response asymmetry for linear accelerations.

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To determine the relative contributions of ampullofugal (AF) and ampullopetal (AP) stimulation of the horizontal semicircular canal (HSCC) to the horizontal vestibulo-ocular reflex (HVOR), 12 patients were studied 1 year after total unilateral vestibular deafferentation (UVD). Compensatory eye movement responses to impulses of horizontal head rotation were studied using magnetic search coils. The head impulses were rapid (up to 3000 deg/sec/sec) passive, unpredictable, step displacements of horizontal angular head position with respect to the trunk.

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Both anatomical and physiological studies have shown that pause neurons (PNs) in the medial pontine reticular formation project to two groups of burst neurons (BNs) involved in the genesis of horizontal saccadic eye movements: The excitatory burst neurons (EBNs), which lie rostral to the abducens nucleus, and the inhibitory burst neurons (IBNs), which lie caudal to the abducens. This study is concerned with the projection from PNs to a group of vertical BNs in the nucleus of the H field of Forel (H FF) in the caudomedial subthalamus. Three anatomical methods were used to demonstrate this connection.

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We examined six patients who developed blurring or oscillopsia as a result of downbeat nystagmus while being treated with lithium carbonate. Of these six plus six previously described similar patients, all but two developed downbeat nystagmus insidiously as an isolated disorder in the setting of otherwise satisfactory therapeutic control, without clinical or biochemical evidence of acute lithium intoxication. Only six of these 12 patients were able either to reduce or to stop taking lithium, and in only two of these six did the downbeat nystagmus improve or remit.

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This paper reviews the literature on the mechanisms responsible for the behavioural recovery which occurs following unilateral labyrinthectomy (UL), UL causes a syndrome of ocular motor and postural disorders, which diminish over time in a process of behavioural recovery known as vestibular compensation. Electrophysiological studies show that the VIIIth nerve does not undergo a functional recovery, therefore vestibular compensation has been attributed to CNS plasticity. However, the nature of the plasticity responsible for vestibular compensation is not understood.

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A new model of otolithic stimulation by linear acceleration is presented and compared to previous models, based upon anatomical evidence and on the ability of normal subjects to sense the direction of a linear acceleration vector acting in the coronal plane (roll-tilt perception). There are two basic methods of generating roll-tilt stimuli: 1) tilt-chairs either inside or outside a centrifuge and 2) fixed-chair centrifuges. The present model is based on consideration of the probable otoconial displacement produced by these two different methods of stimulation and the model incorporates a major role for the elastic restoring force of the otolith membrane.

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The ability of 33 patients to perceive the direction, relative to the body long axis, of a linear acceleration vector acting in the coronal plane, roll-tilt perception, was studied at various times, before and from 1 week to 6 months after unilateral, selective vestibular neurectomy for Meniere's disease, acoustic neuroma or intractable paroxysmal vertigo. The results of these patients were compared with the results of 31 normal subjects and two control patients who had both vestibular nerves surgically sectioned. Rotating on a fixed-chair centrifuge in an otherwise darkened room, each observer was required to indicate his perception of the direction of the resultant gravito-inertial vector by setting a small, motor-driven, illuminated bar, attached to the chair but rotatable in the fronto-parallel plane, to the perceived gravitational horizontal.

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The morphology of horizontal canal second-order type I neurons was investigated by intracellular staining with horseradish peroxidase (HRP) and three-dimensional reconstruction of the cell bodies and axons. Axons penetrated in and around the abducens nucleus were identified as originating from type I neurons by their characteristic firing pattern to horizontal rotation and by their monosynaptic response to stimulation of the ipsilateral vestibular nerve. A total of 47 type I neurons were stained.

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Unilateral loss of horizontal semicircular canal function, termed canal paresis, is an important finding in dizzy patients. To our knowledge, apart from head-shaking nystagmus, no clinical sign of canal paresis has yet been described and the term derives from the characteristic finding on caloric tests: little or no nystagmus evoked by either hot or cold irrigation of the affected ear. We describe a simple and reliable clinical sign of total unilateral loss of horizontal semicircular canal function: one large or several small oppositely directed, compensatory, refixation saccades elicited by rapid horizontal head rotation toward the lesioned side.

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The recovery of normal ocular motor and postural behavior following unilateral labyrinthectomy (vestibular compensation) has been attributed to the return of normal resting activity to neurons in the bilateral vestibular nuclei. However, previous studies in the cat have reported that average resting activity recovers to no more than 50% of the normal value in neurons in the vestibular nucleus ipsilateral to the labyrinthectomy even after 4 months post-operation (post-op.), despite the fact that, for some symptoms, vestibular compensation is complete by this time.

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The recovery of normal ocular motor and postural behavior following unilateral labyrinthectomy is termed vestibular compensation and it has been attributed to the return of normal resting activity to neurons in the bilateral vestibular nuclei. Previous studies in the cat have reported that approximately normal resting activity returns to type I neurons in the medial vestibular nucleus (MVN) contralateral to the deafferentiation by 4-8 weeks post-operation (post-op.), while the gain of the response of these neurons to horizontal angular acceleration remains lower than normal.

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Pause neurons (PNs) are inhibitory neurons close to the midline at the pontomedullary junction that fire tonically and then cease firing just prior to quick eye movements of visual or vestibular origin. Previous physiological evidence has shown that these neurons have a role of central importance in the generation of rapid eye movements in any direction and all major models of ocular motor control incorporate PNs as major elements. In this study in cats, we injected horseradish peroxidase intracellularly into somata or axons of physiologically identified PNs.

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This study investigated the direction of eye movements produced by localized high frequency electrical stimulation of spots on the utricular and saccular macula in lightly anesthetized guinea pigs using fine bipolar stimulating electrodes to minimize current spread and attempting to keep the other labyrinthine sensory regions functional. Threshold stimulating currents produced upward or upward-torsional movements of the ipsilateral eye. There was no evidence of different directions of eye movements corresponding to different hair cell orientations, nor was there evidence of opposite directions of eye movements produced by stimulation on opposite sides of the striola.

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This study provides measurements in individual specimens of the sizes, cross-sectional shapes and areas all around the path of fluid flow through the human horizontal semicircular duct, ampulla and utricle. These data were obtained from multiple measurements on individual specimens which had been fixed by immersion in Karnovsky's fixative and microdis-sected. The results are compared with similar measurements in the rat and guinea pig.

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Anatomic and electrophysiologic evidence suggests there is a vestibular input to eye movement-related pause neurons in the midline of the pontine reticular formation of the cat. The present investigation sought to explore the functional significance of this vestibular drive by examining pause neuron response to horizontal rotational stimulation as cats were anesthetized with halothane or went into natural light sleep. Anesthesia unmasks the vestibular input to pause neurons in that during anesthesia, pause neurons continue to fire but their firing rate is modulated by vestibular stimulation.

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This study provides measurements in individual specimens of the sizes, cross-sectional shapes and areas all around the path of fluid flow through the human horizontal semicircular duct, ampulla and utricle. These data were obtained from multiple measurements on individual specimens which had been fixed by immersion in Karnovsky's fixative and microdissected. The results are compared with similar measurements in the rat and guinea pig.

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The classic Steinhausen/Groen mathematical description of endolymph flow in a toroidal semicircular canal is extended to the case where the size, shape, and curvature of the canal lumen change continuously through the duct, utricle, and ampulla. The resulting second-order differential equation has three coefficients, unlike the equation of a torsion pendulum, which has only two. The salient anatomical parameters which determine endolymph motion are: the length of the central streamline occupying the center of the canal lumen; the area enclosed by this streamline as projected into the plane of rotation; the average inverse cross-sectional area of the lumen (taken around the central streamline); and the average inverse squared cross-sectional area, weighted by a local wall shape factor.

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The rapid recovery from the postural and ocular motor asymmetries produced by unilateral vestibular damage (vestibular compensation) has been presented as an example of plasticity in the central nervous system. A recent model (J. Neurophysiol.

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Brain stem pause neurons play an important role in the regulation of rapid eye movements. However, the input sources that drive pause neurons are uncertain. In the present study, horizontal canal type II neurons in the medial vestibular nucleus were antidromically activated by electrical stimulation of the pause neuron region.

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Total visual deprivation has no effect on the level of compensation of spontaneous nystagmus and lateral head deviation attained by 52 h after labyrinthectomy in the guinea pig. However, compensation of longitudinal twisting is significantly reduced. It is concluded that the role of vision in vestibular compensation may be specific to species and, in the guinea pig, to longitudinal twisting.

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