Automatic detection and removal of fast phases from nystagmographic recordings by optimal thresholding

Recording of ocular nystagmus during vestibular tests does not measure the true response of the vestibulo-ocular reflex (VOR), because the VOR response (so-called slow phase of nystagmus) is interrupted by resetting saccades (so-called fast phase of nystagmus). In order to extract the real VOR contribution, saccades must be removed. In most of the nystagmus processing algorithms, saccade removal requires a human operator to choose a suitable eye velocity threshold able to separate fast from slow nystagmus phases. In the present report a fully automatic removal system is presented which selects an optimal velocity threshold by computing the VOR frequency response and maximizing its coherence function.     

Development of Eye Position Dependency of Slow Phase Velocity during Caloric Stimulation

The nystagmus in patients with vestibular disorders often has an eye position dependency, called Alexander’s law, where the slow phase velocity is higher with gaze in the fast phase direction compared with gaze in the slow phase direction. Alexander’s law has been hypothesized to arise either due to adaptive changes in the velocity-to-position neural integrator, or as a consequence of processing of the vestibular-ocular reflex. We tested whether Alexander’s law arises only as a consequence of non-physiologic vestibular stimulation. We measured the time course of the development of Alexander’s law in healthy humans with nystagmus caused by three types of caloric vestibular stimulation: cold (unilateral inhibition), warm (unilateral excitation), and simultaneous bilateral bithermal (one side cold, the other warm) stimulation, mimicking the normal push-pull pattern of vestibular stimulation. Alexander’s law, measured as a negative slope of the velocity versus position curve, was observed in all conditions. A reversed pattern of eye position dependency (positive slope) was found <10% of the time. The slope often changed with nystagmus velocity (cross-correlation of nystagmus speed and slope was significant in 50% of cases), and the average lag of the slope with the speed was not significantly different from zero. Our results do not support the hypothesis that Alexander’s law can only be observed with non-physiologic vestibular stimulation. Further, the rapid development of Alexander’s law, while possible for an adaptive mechanism, is nonetheless quite fast compared to most other ocular motor adaptations. These results suggest that Alexander’s law may not be a consequence of a true adaptive mechanism.     

On the predominance of anti-compensatory eye movements in vestibular nystagmus

The predominance of anti-compensatory eye movements in vestibular nystagmus recorded during sinusoidal and post-rotational tests is interpreted in terms of a mathematical model of the vestibulo-ocular system. Namely, a direct pathway between the vestibular nuclei and the saccadic mechanism is assumed. In the range of frequencies of natural head movements this pathway carries on a signal proportional to head angular velocity. Therefore, during active head movements the saccadic mechanism is forced to produce quick eye rotations in the direction of head movement and, thus, to cooperate in the task of picking up visual targets outside the visual field. During passive head movements giving rise to nystagmus the assumed pathway contributes to reduce the error in eye resetting due to the saccadic delay. Analytical considerations and simulation results seem to prove the adequacy of the proposed model.Work supported by the National Research Council (C.N.R.), Rome, Italy     

A new light on caloric test--what was disclosed by three dimensional analysis of caloric nystagmus?

For better understanding of caloric nystagmus, this phenomenon will be reviewed historically in three stages. 1) The first light on caloric nystagmus was thrown by Barany 1906. Through direct observation of eye movements, Barany established the caloric test as an important tool to determine the side of lesion for vertigo. 2) The second light is shed by electrooculogram (EOG) from the late 1950th. EOG enabled qualitative analysis of caloric nystagmus, and proved Barany's convection theory, but resulted in neglect of vertical and roll eye movements. 3) The third light is gained by 3D recording of eye movements started from the late 1980th. 3D recordings of eye movements enabled us to analyze the spatial orientation of caloric nystagmus, and disclose the close correlation of the nystagmus components in the head vertical and the space vertical planes, suggesting a contribution of the velocity storage integrator. The 3D property of caloric nystagmus will be explained in detail.     

Fast component threshold for vestibular nystagmus in the rabbit

The existence of a threshold for the production of fast components of vestibular nystagmus was investigated in the rabbit. The characteristics (position and velocity) of reflexive eye movements were precisely monitored with the use of the search-coil method and a laboratory computer. The threshold largely depended on the eye position in the orbit during nystagmus and, to a much lesser extent, on the eye velocity. The basic characteristics of the threshold remained unchanged under vestibular stimulation in the dark and in the light, and for different frequencies and peak velocities of rotation. A pattern of vestibular nystagmus was demonstrated whereby it is possible to predict the occurrence of fast components.     

Modern Tests of Vestibular Function,with Special Reference to their Value in Clinical Practice

The many vestibular tests now available provide the means of accurate localization of lesions at all levels of the vestibular pathways. The value of the test procedures described has been well established in the examination of very many patients over the past twenty years, and though other forms of tests are available only those have been included which have proved to give consistently useful information.Most of these tests can be undertaken by the clinician without the use of any costly equipment, and together with a careful history and examination the diagnosis can in most cases be arrived at. Recognition of the highly important role of optic fixation and ocular deviations on vestibular nystagmus, together with recent facilities to demonstrate this electronystagmographically, may provide additional valuable and more precise information.     

视频眼震检查在主诉非典型眩晕患者中的临床应用价值

目的:探讨视频眼震检查在主诉非典型眩晕患者中的临床应用价值。方法:分析118例主诉非典型眩晕患者的裸眼眼震、视频眼震,结合查体、已有的或者后续的双温试验、听力学检查以及影像学等临床资料,评估视频眼震检查的应用对前庭疾病临床诊断的意义。结果:主诉持续头昏沉感患者10例、飘飘感23例;低头、抬头、坐起、躺下、翻身等头部位置改变时不穏感50例;或者上述动作引起瞬间旋转感35例。以上患者均行自发性眼震检查和位置试验,裸眼下观察到眼震的患者有19例(19/118,16.1%),均得到临床诊断;视频下记录到眼震67例(67/118,56.8%),其中60例(60/118,50.8%)得出临床诊断。两种方法的眼震检出率比较差异有显著的统计学意义(P0.05),视频眼震检查的检出率显著高于裸眼下观察。结论:视频眼震检查所采用的眼罩有暗室诱发的效果,方便快捷,较裸眼观察,可显著地增加以下几种主诉非典型(转头时飘飘感,低头、抬头、坐起、躺下、翻身等头部位置改变时不穏感或者瞬间旋转感)眩晕患者眼震的临床诱发率,提供进一步的诊查方向,提高临床上对主诉非典型眩晕患者的诊断率。     

Role of NMDA receptors in the compensation of ocular nystagmus induced by hemilabyrinthectomy in the guinea pig.

The possibility that N-methyl-D-aspartate (NMDA) receptor activation plays a role in inducing the vestibular compensation following hemilabyrinthectomy (HL) in guinea pigs, was verified by means of continuous intraventricular osmotic pumping of DL-2-Amino-5-phosphono-valeric acid (APV). Our results show that high doses (40 and 20 mM) of APV decrease both the combined OKR and VOR and the nystagmus following HL. Low doses of APV (2.5 mM), affect the time course of the ocular compensation by maintaining a higher level of nystagmus beat frequency and by delaying the nystagmus disappearance. On the contrary, the compensation time course is not affected by administering APV later on in the compensation period. Therefore, it appears that NMDA receptors are activated during the precocious phase of vestibular compensation, when a large vestibular imbalance is present. This finding is explained by the development of NMDA receptor hypersensitivity, in the functionally inactivated commissural system or by the occurrence of NMDA-mediated long-term potentiation.     

Dizziness and Head Injury

Dizziness, whether vague or specifically rotational, is a common sequel to head injury, and is often postural. One hundred and sixty-five patients with this symptom were examined. The simple posture tests employed to detect positional nystagmus are described. This physical finding was present in one-quarter of the entire group, and in nearly one-half of cases of longitudinal fracture of temporal bone. In such cases, it is an objective finding that corresponds precisely to the patient''s complaint of vertigo.Transverse fracture of temporal bone destroys the inner ear in both cochlear and vestibular parts. Longitudinal fracture is commoner and causes bleeding from the ear; inner-ear damage is usually minor.In the rare cases where persisting postural vertigo and positional nystagmus are disabling, relief of the symptom may be achieved by vestibular denervation of the affected side.     

Compensatory processes during unilateral loss of vestibular function]

Changes in the compensation of the sequences of the unilateral loss of the labyrinthine function were studied in rabbits. Destruction of the labyrinth was accompanied by ocular nystagmus, increase of frequency of respiration and heart contractions, and EEG-activation. Investigations carried out showed these reactions to be extinguished at different time. At the late periods of labyrinthectomy a considerable asymmetry of nystagmus reaction to the angular accelerations equal in intensity, but opposite in direction was revealed. Stimulation of an intact otolith labyrinth was accompanied by the appearance of positional nystagmus. The results obtained indicated imperfection of the compensatory mechanisms during complete unilateral loss of the vestibular function.     

Time constants of vestibular nuclei neurons in the goldfish: A model with ocular proprioception

A simple model of the vestibular-ocular reflex with a proprioceptive eye velocity feedback loop is used to simulate recent data on the vestibular responses of neurons in the vestibular nuclei of spinal goldfish. The data support the hypothesis that a proprioceptive feedback loop elongates the vestibular nucleus time constant to equal that of the slow phase eye movements of vestibular nystagmus.     

Convergence rotatory nystagmus under unusual conditions of semicircular canal and otolith stimulation

The characteristics of interaction between two vestibular subsystems (otiliths and semicircular canals) were studied by means of binocular (bilateral) videooculographic recording of eye movements in 43 men aged from 19 to 41 years that had been found healthy upon aviation physical examination. The time course of horizontal vestibular nystagmus was analyzed separately for each eye in subjects who bent forward and straightened up in the sagittal plane while being rotated about the vertical body axis in an electrically driven rotating chair. This combined rotation caused interocular asymmetric nystagmus in 91% of the subjects and convergence rotatory nystagmus in 42% of the subjects. A hypothesis on the mechanism of interocular asymmetric nystagmus caused by the combined rotation and convergence rotatory nystagmus as its special case has been advanced. The hypothesis allows for independent nystagmic mechanisms (subsystems) for the right and left eyes.     

On the Vertigo Due to Static Magnetic Fields

Vertigo is sometimes experienced in and around MRI scanners. Mechanisms involving stimulation of the vestibular system by movement in magnetic fields or magnetic field spatial gradients have been proposed. However, it was recently shown that vestibular-dependent ocular nystagmus is evoked when stationary in homogenous static magnetic fields. The proposed mechanism involves Lorentz forces acting on endolymph to deflect semicircular canal (SCC) cupulae. To investigate whether vertigo arises from a similar mechanism we recorded qualitative and quantitative aspects of vertigo and 2D eye movements from supine healthy adults (n = 25) deprived of vision while pushed into the 7T static field of an MRI scanner. Exposures were variable and included up to 135s stationary at 7T. Nystagmus was mainly horizontal, persisted during long-exposures with partial decline, and reversed upon withdrawal. The dominant vertiginous perception with the head facing up was rotation in the horizontal plane (85% incidence) with a consistent direction across participants. With the head turned 90 degrees in yaw the perception did not transform into equivalent vertical plane rotation, indicating a context-dependency of the perception. During long exposures, illusory rotation lasted on average 50 s, including 42 s whilst stationary at 7T. Upon withdrawal, perception re-emerged and reversed, lasting on average 30 s. Onset fields for nystagmus and perception were significantly correlated (p<.05). Although perception did not persist as long as nystagmus, this is a known feature of continuous SSC stimulation. These observations, and others in the paper, are compatible with magnetic-field evoked-vertigo and nystagmus sharing a common mechanism. With this interpretation, response decay and reversal upon withdrawal from the field, are due to adaptation to continuous vestibular input. Although the study does not entirely exclude the possibility of mechanisms involving transient vestibular stimulation during movement in and out of the bore, we argue these are less likely.     

POSTURAL VERTIGO AND POSITIONAL NYSTAGMUS

Oscillation of the eyes of a patient when the head is placed in a certain position is objective evidence to support a complaint of postural vertigo—dizziness when the head is tilted forward or upward or turned to one side or the other. Since positional nystagmus may be difficult to evoke and may be elicited at one time and not at another, it is important to make repeated tests, lest a causative lesion be overlooked.Vertigo in such cases may be caused by pathologic change in the eighth peripheral nerve or in the central vestibular pathways. Sometimes no organic disease is observable even though positional nystagmus validates a complaint of vertigo. In such instances the patient should be assured that he does not have a progressive disease and be advised against activity in which dizziness would be hazardous.     

A model of Alexander's law of vestibular nystagmus

The observation that the amplitude of vestibular nystagmus grows as gaze is increased in the direction of the nystagmus fast phase and diminished with gaze in the opposite direction is known as Alexander's law. We have developed an analog computer model to simulate Alexander's law in nystagmus secondary to dysfunction of a semicircular canal. The model utilizes relevant brainstem anatomy and physiology and includes gaze modulation of vestibular signals and push-pull integration to create eye positition commands. When simulating normally functioning semicircular canals, the model produced no nystagmus. When simulating total impairment of the canal on one side with gaze directed maximally in the opposite direction, the model produced a large amplitude nystagmus with linear slow phases directed toward the affected side. As gaze was changed from far contralateral to ipsilateral, the nystagmus gradually diminished to zero. When simulating partial impairment of one canal, the nystagmus was smaller in amplitude and absent in ipsilateral gaze.     

A random walk model of fast-phase timing during optokinetic nystagmus

 Most vertebrate animals produce optokinetic nystagmus in response to rotation of their visual surround. Nystagmus consists of an alternation of slow-phase eye rotations, which follow the surround, and fast-phase eye rotations, which quickly reset eye position. The time intervals between fast phases vary stochastically, even during optokinetic nystagmus produced by constant velocity rotation of a uniform surround. The inter-fast-phase interval distribution has a long tail, and intervals that are long relative to the mode become even more likely as constant surround velocity is decreased. This paper provides insight into fast-phase timing by showing that the process of fast-phase generation during constant velocity optokinetic nystagmus is analogous to a random walk with drift toward a threshold. Neurophysiologically, the output of vestibular nucleus neurons, which drive the slow phase, would approximate a random walk with drift because they integrate the noisy, constant surround velocity signal they receive from the visual system. Burst neurons, which fire a burst to drive the fast phase and reset the slow phase, are brought to threshold by the vestibular nucleus neurons. Such a nystagmic process produces stochastically varying inter-fast-phase intervals, and long intervals emerge naturally because, as drift rate (related to surround velocity) decreases, it becomes more likely that any random walk can meander for a long time before it crosses the threshold. The theoretical probability density function of the first threshold crossing times of random walks with drift is known to be that of an inverse Gaussian distribution. This probability density function describes well the distributions of the intervals between fast phases that were either determined experimentally, or simulated using a neurophysiologically plausible neural network model of fast-phase generation, during constant velocity optokinetic nystagmus. Received: 1 June 1995/Accepted in revised form: 15 February 1996     

A burst-feedback model of fast-phase burst generation during nystagmus

 Vestibular and optokinetic nystagmus are characterized by alternating slow-phase eye rotations that stabilize the retinal image, and fast-phase eye rotations that reset eye position. Nystagmus is coordinated in the brainstem by burst neurons that fire an intense, temporally circumscribed burst that terminates the slow phase and drives the fast phase. This paper demonstrates that such a burst can be generated during nystagmus using a simple neural network model containing only known brainstem neurons and their interconnections. These include the feedback connections of the burst neuron (burst feedback). The burst neuron excites itself directly, and disinhibits itself by inhibiting the pause neuron (positive feedback). It also inhibits itself by inhibiting the vestibular neuron (negative feedback). The burst neuron begins to fire after its inhibitory bias is overcome by excitation from the vestibular neuron, and burst neuron positive feedback then produces an intense burst with an abrupt onset. The burst causes the vestibular and pause neurons to pause. The benefit of the pause neuron loop is that it contributes to burst neuron positive feedback when it is needed at burst onset, but that contribution is eliminated when the pause neuron pauses and opens the loop. The burst can then terminate, with an offset duration proportional to burst amplitude, under the control of burst neuron self-excitation and inhibitory bias. Model neuron behavior is comparable to that of real brainstem neurons. Synchronized bursts can be produced over the population of burst neurons in a distributed version of the network. Variability in connection weights in the distributed network results in variability in prelude activity among burst neurons that is similar to the spread in lead observed for real burst neurons during nystagmus. Received: 11 April 1996 / Accepted in revised form: 6 August 1996     

Neurogenic potential of the vestibular nuclei and behavioural recovery time course in the adult cat are governed by the nature of the vestibular damage

Functional and reactive neurogenesis and astrogenesis are observed in deafferented vestibular nuclei after unilateral vestibular nerve section in adult cats. The newborn cells survive up to one month and contribute actively to the successful recovery of posturo-locomotor functions. This study investigates whether the nature of vestibular deafferentation has an incidence on the neurogenic potential of the vestibular nuclei, and on the time course of behavioural recovery. Three animal models that mimic different vestibular pathologies were used: unilateral and permanent suppression of vestibular input by unilateral vestibular neurectomy (UVN), or by unilateral labyrinthectomy (UL, the mechanical destruction of peripheral vestibular receptors), or unilateral and reversible blockade of vestibular nerve input using tetrodotoxin (TTX). Neurogenesis and astrogenesis were revealed in the vestibular nuclei using bromodeoxyuridine (BrdU) as a newborn cell marker, while glial fibrillary acidic protein (GFAP) and glutamate decarboxylase 67 (GAD67) were used to identify astrocytes and GABAergic neurons, respectively. Spontaneous nystagmus and posturo-locomotor tests (static and dynamic balance performance) were carried out to quantify the behavioural recovery process. Results showed that the nature of vestibular loss determined the cellular plastic events occurring in the vestibular nuclei and affected the time course of behavioural recovery. Interestingly, the deafferented vestibular nuclei express neurogenic potential after acute and total vestibular loss only (UVN), while non-structural plastic processes are involved when the vestibular deafferentation is less drastic (UL, TTX). This is the first experimental evidence that the vestibular complex in the brainstem can become neurogenic under specific injury. These new data are of interest for understanding the factors favouring the expression of functional neurogenesis in adult mammals in a brain repair perspective, and are of clinical relevance in vestibular pathology.     

Modeling the interaction among three cerebellar disorders of eye movements: periodic alternating,gaze-evoked and rebound nystagmus

A woman, age 44, with a positive anti-YO paraneoplastic cerebellar syndrome and normal imaging developed an ocular motor disorder including periodic alternating nystagmus (PAN), gaze-evoked nystagmus (GEN) and rebound nystagmus (RN). During fixation there was typical PAN but changes in gaze position evoked complex, time-varying oscillations of GEN and RN. To unravel the pathophysiology of this unusual pattern of nystagmus, we developed a mathematical model of normal function of the circuits mediating the vestibular-ocular reflex and gaze-holding including their adaptive mechanisms. Simulations showed that all the findings of our patient could be explained by two, small, isolated changes in cerebellar circuits: reducing the time constant of the gaze-holding integrator, producing GEN and RN, and increasing the gain of the vestibular velocity-storage positive feedback loop, producing PAN. We conclude that the gaze- and time-varying pattern of nystagmus in our patient can be accounted for by superposition of one model that produces typical PAN and another model that produces typical GEN and RN, without requiring a new oscillator in the gaze-holding system or a more complex, nonlinear interaction between the two models. This analysis suggest a strategy for uncovering gaze-evoked and rebound nystagmus in the setting of a time-varying nystagmus such as PAN. Our results are also consistent with current ideas of compartmentalization of cerebellar functions for the control of the vestibular velocity-storage mechanism (nodulus and ventral uvula) and for holding horizontal gaze steady (the flocculus and tonsil).