Impairment of optokinetic (after-)nystagmus by labyrinthectomy in the rabbit

After bilateral labyrinthectomy the maximal slow-phase velocity of optokinetic nystagmus was limited to a few degrees/sec. Optokinetic tracking of rotation at speeds up to 1 to 3°/sec was entirely normal, but the usual gradual increase of slow-phase velocity induced by faster rotation (up to 30 to 60°/sec) was absent. Also optokinetic stimulation under open-loop conditions and electrical stimulation of the optokinetic pathway were unable to generate faster pursuit. Optokinetic after-nystagmus was entirely abolished. These results indicate a duality in optokinetic reactions: a direct response to slow retinal image displacement (e.g., drift), and an indirect response, mediated through the vestibular system, to faster movements.     

Effect of roll and pitch on flash-induced nystagmus: Support for involvement of retinal direction-selective elements?

The direction of eye movement (i.e., the angle of the resultant velocity vector calculated from the horizontal and vertical components) during flash-induced nystagmus was evaluated in static roll and pitch positions. It appeared that this direction coincided with the orientation of the visual streak, as influenced by the ocular countertorsion which is known to occur in the various body positions. This supports the hypothesis that flash-induced nystagmus results from stimulation of direction-selective retinal elements. The intensity of flash-induced nystagmus, evaluated either by measuring slow-phase velocity (i.e., magnitude of resultant vector) or by beat frequency, was minimal in approximately 90 and 270 degrees roll or pitch positions, presumably because the total combined (utricular and saccular, left and right) excitatory otolith stimulation was maximal in these positions, the effect of this stimulation being inhibitory to the flash-induced nystagmus.     

Ginkgolide B accelerates vestibular compensation of spontaneous ocular nystagmus in guinea pig following unilateral labyrinthectomy

The aim of this study was to investigate the effects of ginkgolide B on the behavioral recovery process (vestibular compensation) which occurs following surgical removal of the vestibular receptor cells in one labyrinth (unilateral labyrinthectomy, UL). Guinea pigs received a single ip injection of ginkgolide B at the time of the UL (25, 50, or 100 mg/kg) and the effects on the compensation of the UL symptoms, spontaneous ocular nystagmus (SN), yaw head tilt (YHT), and roll head tilt (RHT), were evaluated. The effects of a single vehicle injection or a similar injection of ginkgolide A were used for comparison. Twenty-five mg/kg ginkgolide B significantly increased the rate of SN compensation compared to the vehicle control group (P < 0.02). However, 50 mg/kg ginkgolide B had no significant effect on either SN frequency or the rate of SN compensation. Ginkgolide B (100 mg/kg) significantly altered the rate of SN compensation (P < 0.02); however, SN frequency values were higher at most measurement times. YHT and RHT were not significantly affected by ginkgolide B at any of the doses used. Twenty-five mg/kg ginkgolide A had no significant effect on any of the UL symptoms. These results suggest that, at the optimal dose of 25 mg/kg, a single ip injection of ginkgolide B at the time of the UL can produce an acceleration of SN compensation.     

The effect of hyperventilation on downbeat nystagmus in cerebellar disorders.

Hyperventilation can affect nystagmus in patients with vestibular disorders. However, the effects on nystagmus in patients with cerebellar disease have not been systematically studied. Using the magnetic field search coil technique, we studied the effects of hyperventilation on nystagmus in a series of cerebellar patients. In four of eight patients, hyperventilation produced an increase in the slow-phase velocity of downbeat nystagmus. We speculate that this effect may be mediated through metabolic effects on cerebellar calcium channels.     

The influence of age on optokinetic nystagmus

Summary The influence of age on optokinetic nystagmus (OKN) was studied in 63 healthy subjects, who were divided into three groups according to their age, group I (20–39 years), 11 (40–59 years) and III (60–82 years). It was found that on average maximal OKN velocity decreases considerably with age, from 114°/s in group I to 93°/s in group II and 73°/s in group III.Two mechanisms participate in the generation of OKN, the so-called fast component and velocity storage component. The fast component leads to immediate changes in slow phase nystagmus velocity and is related to smooth pursuit eye movements. The velocity storage component causes more gradual velocity changes and expresses itself during optokinetic afternystagmus (OKAN). To study the relative contribution of these two components, maximal smooth pursuit and OKAN velocity were determined in addition to the maximal OKN velocity for the same individuals. It was found that both smooth pursuit and OKAN performance decrease with age. Consequently the maximal OKN velocity, which depends on both factors, is even more affected than smooth pursuit eye movements.Supported by Deutsche Forschungsgemeinschaft SFB 200, A2     

The nystagmus of vestibular paroxysmia

Journal of Neurology -     

Periodic lateralized epileptiform discharges (PLED's) and nystagmus retractorius.

A 57-year-old diabetic woman presented with focal right-sided seizures and hyperglycemia. She later showed periodic lateralized epileptiform discharges (PLEDs), originating in the left hemisphere, which were temporally associated with nystagmus retractorius. It appears that the left hemisphere epileptiform activity diffusely excited brainstem structures via polysynaptic pathways to produce the nystagmus.