Transient analysis of vestibular nystagmus

The significance of a nystagmus-dependent, transient component in the overall slow-phase response of the vestibulo-ocular reflex (VOR) is brought into focus. First, a simulated example is presented that shows how this transient component can bias current algorithms for the estimation of VOR parameters. Second, new algorithms are proposed that are able to estimate VOR parameters regardless of the presence of transients. Third, the new algorithms are applied to experimental data, and the results are compared with those from current algorithms. The results clearly show that the transient component can significantly alter the apparent VOR time constant, particularly when the reflex has been lesioned. The algorithms open new areas of research on the possible role of nystagmus in enhancing the compensatory function of the VOR.     

Interaction between vision and vestibular nystagmus]

In order to assess the visuo-vestibular interaction and its behaviour in connection with the age, we have submitted 20 healthy subjects from two age groups ranging between 21-30 and 65-75 years of age to two rotation tests (with closed eyes and with opened eyes with fixation of a light). The results show a variation of the nystagmic response with fixation of about 60% in the young people and of about 40% in the elderly. These results demonstrate that the extent of the inhibition is dependent upon age and is less effective in the elderly.     

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.     

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.     

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     

On the distribution of fast-phase intervals in optokinetic and vestibular nystagmus

 Histograms of fast-phase intervals in human optokinetic and vestibular nystagmus were generated, and fitted to statistical distributions used in previous studies. The distributions did not depend on stimulation type (optokinetic or vestibular). An inverse Gaussian or a gamma distribution fitted the data better than did a reciprocal Gaussian distribution, but none fitted the data especially well. In some cases, however, the interpretation of these distributions is more physiologically satisfactory than in others. Recommendations are made on which class of models is preferred, and the experiments needed to support the particular models. Our results call into question the validity of previous studies that fit statistical distributions to data sets of a size comparable to ours. Received: 26 June 2001 / Accepted in revised form: 20 February 2002     

Nonlinear time series analysis of jerk congenital nystagmus

Nonlinear dynamics provides a complementary framework to control theory for the quantitative analysis of the oculomotor control system. This paper presents a number of findings relating to the aetiology and mechanics of the pathological ocular oscillation jerk congenital nystagmus (jerk CN). A range of time series analysis techniques were applied to recorded jerk CN waveforms, and also to simulated jerk waveforms produced by an established model in which the oscillations are a consequence of an unstable neural integrator. The results of the analysis were then interpreted within the framework of a generalised model of the unforced oculomotor system. This work suggests that for jerk oscillations, the origin of the instability lies in one of the five oculomotor subsystems, rather than in the final common pathway (the neural integrator and muscle plant). Additionally, experimental estimates of the linearised foveation dynamics imply that a refixating fast phase induced by a near-homoclinic trajectory will result in periodic oscillations. Local dimension calculations show that the dimension of the experimental jerk CN data increases during the fast phase, indicating that the oscillations are not periodic, and hence that the refixation mechanism is of greater complexity than a homoclinic reinjection. The dimension increase is hypothesised to result either from a signal-dependent noise process in the saccadic system, or the activation of additional oculomotor components at the beginning of the fast phase. The modification of a recent saccadic system model to incorporate biologically realistic signal-dependent noise is suggested, in order to test the first of these hypotheses. Action Editor: Peter Latham