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Query: UMLS:C0028738 (nystagmus)
 7,431 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Horizontal and vertical optokinetic nystagmus (OKN) and optokinetic after-nystagmus (OKAN) of squirrel monkeys were compared with those of rabbits, cats and humans that were previously described. Squirrel monkeys showed similar findings to cats, in which vertical optokinetic nystagmus (VOKN) is not as well elicited as horizontal optokinetic nystagmus (HOKN) and down-pursuit OKN is poorer than up-pursuit OKN. As to the reasons that bring about different responses of OKN and OKAN (and vestibular nystagmus) in different planes, we speculated two possibilities: compensatory activation of horizontal eye movement for narrowed visual field accompanied by frontally positioned eyes, and the gravity that restricts and modifies posture and locomotion. Directional difference of VOKN may be caused by a physiological mechanism that makes visual fixation not susceptible to downward movement of the ground surface during forward locomotion.
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PMID:Comparison of vertical and horizontal optokinetic nystagmus in the squirrel monkey. 9 9

Vestibular and optokinetic nystagmus (OKN) of monkeys were induced by platform and visual surround rotation. Vision prolonged per-rotatory nystagmus and cancelled or reduced post-rotatory nystagmus recorded in darkness. Presumably, activity stored during OKN summed with activity arising in the semicircular canals. The limit of summation was about 120 degrees/s, the level of saturation of optokinetic after-nystagmus (OKAN). OKN and vestibular nystagmus, induced in the same or in opposite directions diminished or enhanced post-rotatory nystagmus up to 120 degrees/s. We postulate that a common storage mechanism is used for producing vestibular nystagmus, OKN, and OKAN. Evidence for this is the similar time course of vestibular nystagmus and OKAN and their summation. In addition, stored activity is lost in a similar way by viewing a stationary surround during either OKAN or vestibular nystagmus (fixation suppression). These responses were modelled using direct pathways and a non-ideal integrator coupled to the visual and peripheral vestibular systems. The direct pathways are responsible for rapid changes in eye velocity while the integrator stores activity and mediates slower changes. The integrator stabilizes eye velocity during whole field rotation and extends the time over which the vestibulo-ocular reflex can compensate for head movement.
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PMID:Velocity storage in the vestibulo-ocular reflex arc (VOR). 10 22

Single neurons were recorded in the vestibular nuclei of monkeys trained to suppress nystagmus by visual fixation during vestibular or optokinetic stimulation. During optokinetic nystagmus vestibular nuclei neurons exhibit frequency changes. With the suppression of optokinetic nystagmus this neuronal activity on average is attenuated by 40% at stimulus velocities of 40 degrees/s. At a stimulus velocity of 5 degrees/s responses are, under both conditions, close to threshold. For steps in velocity, suppression of vestibular nystagmus shortens the time constants of the decay of neuronal activity from 15--35 s to 5--9 s, while the amplitude of the response remains unchanged. The results are discussed in relation to current models of visual-vestibular interaction. These models use a feedback mechanism which normally operates during vestibular and optokinetic nystagmus. Nystagmus suppression interrupts this feedback loop.
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PMID:Vestibular nuclei activity in the alert monkey during suppression of vestibular and optokinetic nystagmus. 11 47

We wanted to ascertain whether a physiological horizontal vestibular spontaneous nystagmus is existent, or whether the spontaneous and positional nystagmus seen in clinically healthy persons in the electronystagmogram -- when fixation had been excluded completely -- was always the result of earlier damages to the vestibular system (Jatho). For this purpose we tried to detect a spontaneous and positional nystagmus in 102 healthy persons from 6 age groups (17 each) between 11 and 70 years of age. When the ENG was registered with open eyes in darkness, 63 out of the 102 test persons had a horizontal spontaneous or positional nystagmus, however, under the Frenzel glasses there was a nystagmus in only 2 out of these test persons. With open eyes in darkness, the frequency and intensity was the same in all age groups. With this, we believe to have proved that a physiological horizontal vestibular nystagmus does exist. We share Kornhuber's opinion that the examination with the Frenzel glasses in a dark room, together with the head shaking test and positional test, at the present time represents the best method for differentiating between physiological and pathological spontaneous nystagmus.
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PMID:Spontaneous and positional nystagmus in healthy persons demonstrated only by electronystagmography: physiological spontaneous nystagmus or "functional scar"? 30 84

Several effects of alcohol on vestibular nystagmus are well known, including positional alcoholic nystagmus, a depressive effect on post-rotatory nystagmus, and an inhibition of visual fixation. This study concerns the influence of alcohol on central vestibular compensatory phenomena. In one experiment, hemilabyrinthectomized cats were allowed to compensate for the postoperative spontaneous nystagmus and directional preponderance of post-rotatory nystagmus. Following alcohol injection, spontaneous nystagmus reappeared toward the intact side, positional nystagmus was unidirectional, and post-rotatory nystagmus was profoundly more depressed than for normals. Normal cats subjected to repeated accelerations showed less habituation of post-rotatory nystagmus with alcohol than without.
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PMID:Action of alcohol on vestibular compensation and habituation in the cat. 30 24

A testing of usefulness of systematic search for spontaneous and provoked nystagmus relative to the duration of effect of several hypnotics and narcotics showed in 83% positive vestibular findings in 150 non-selected, ear sound patients. Vestibular nystagmus was still detected 2 hour p.o. in 74%, 3 hours p.o. in 30% and 4 hours p.o. in 7% of cases. 78 times (52%) a convergent or divergent posture nystagmus was recorded and 47 times (31%) a vertical nystagmus. The subjective sensations of the test persons are out of proportion to the objective findings. The localisation of the pharmacotoxic lesion is discussed.
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PMID:[Spontaneous and provoked nystagmus as a criterion of the duration of effect of hypnotics and narcotics in ambulant surgery (author's transl)]. 30

The intersaccadic interval analysis of vestibular nystagmus was proposed by Cheng et al. in 1974. This method gives a statistical and sequential description of intersaccadic intervals. Until now there were no reports concerning the clinical diagnostic relevance of this method in vestibular disturbancies. Therefore, we checked 8 normal probands and 7 patients (3 peripheral, 3 central vestibular lesions, one congenital nystagmus). Compared to common nystagmus parameters like maximum speed of slow phase or minimum frequency normal probands showed a relatively high variability, as well as the patients - excluding congenital nystagmus. The maximum of intersaccadic intervals of the latter was very marked between 0,9 and 1,0 seconds. In the other cases the normally monomodal distributed maxima were between 0,2 and 0,6 sec. A multimodal distribution, as described by Cheng et al. in 1974, were to be found very seldomly. The comparison of intersaccadic interval analysis with the common nystagmus parameters showed, that in clinical diagnostic this method should not be too necessary. However, regarding scientific research - including mathematical models of vestibular nystagmus - the intersaccadic interval analysis could be useful.
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PMID:[How useful is the intersaccadic interval analysis of vestibular nystagmus for clinical diagnostic (author's transl)]. 31 14

The interaction of vestibular and optokinetic nystagmus (OKN) was investigated by applying periods of ipsi- and contradirectional optokinetic stimulation during perand postrotatory vestibular nystagmus in healthy humans. Slow phase velocity and cumulative eye displacement of OKN was enhanced by vestibular nystagmus beating in the same direction of decreased by contradirectional vestibular nystagmus. A distinct correlation between the intensity of vestibular stimulation and the modification of OKN could be demonstrated by averaging the responses obtained in different subjects. On the other hand there was also a modification (enhancement or decrease) of vestibular nystagmus slow phase velocity by preceding OKN. Considering the intensity of these modifications, large interindividual differences were observed.
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PMID:On the interaction of vestibular and optokinetic nystagmus in man. 31 14

The effect of ethacrynic acid (ETA) upon pendular rotation nystagmus and paralytic nystagmus was examined using 61 guinea pigs. 100 mg/kg ETA reduced these nystagmus but 30 mg/kg ETA had on effect. Galvanic nystagmus, Bechterew's compensatory nystagmus, OKN and EEG were not affected by 100 ng/kg ETA. These results are highly suggestive that the inhibition of the peripheral vestibular nystagmus by ETA is mainly due to the reduction of the ampullar endolymphatic potential.
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PMID:Effect of ethacrynic acid upon the peripheral vestibular nystagmus. 31 40

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 position 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.
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PMID:A model of Alexander's law of vestibular nystagmus. 31 22


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