PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Nystagmus”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1977

Spontaneous and positional nystagmus in healthy persons demonstrated only by electronystagmography: physiological spontaneous nystagmus or "functional scar"?

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.

Adolescent↗
PubMed1979

Slow build-up of optokinetic nystagmus associated with downbeat nystagmus.

Eye movement recordings in two patients with downbeat nystagmus demonstrated an unusual finding of severely impaired smooth pursuit and relatively unimpaired optokinetic nystagmus (OKN). OKN was characterized by a remarkable, slow build-up of slow-component velocity, similar to that found in afoveate animals. Optokinetic after-nystagmus (OKAN), or transient persistence of nystagmus after cessation of visual stimulation, typical of the optokinetic response of normal human subjects, was also preserved in these patients. These observations suggest that the normal contribution of smooth pursuit to the ocular motor response to rotation of the visual environment can be selectively removed by a lesion at the level of the craniocervical junction.

Adult↗
PubMed1977

Quantitative analysis of the velocity characteristics of optokinetic nystagmus and optokinetic after-nystagmus.

1. Velocity characteristics of optokinetic nystagmus (OKN) and optokinetic after-nystagmus (OKAN) induced by constant velocity full field rotation were studied in rhesus monkeys. A technique is described for estimating the dominant time constant of slow phase velocity curves and of monotonically changing data. Time constants obtained by this technique were used in formulating a model of the mechanism responsible for producing OKN and OKAN.2. Slow phase velocity of optokinetic nystagmus in response to steps in stimulus velocity was shown to be composed of two components, a rapid rise, followed by a slower rise to a steady-state value. Peak values of OKN slow phase velocity increased linearly with increases in stimulus velocity to 180 degrees /sec. Maximum slow phase eye velocities in the monkey are 2-3 times as great as in humans.3. At the onset of OKAN, slow phase velocity falls by about 10-20%, followed by a slower decline to zero. Peak OKAN slow phase velocities were linearly related to optokinetic stimulus velocities up to 90-120 degrees /sec. Above 120 degrees /sec OKAN slow phase velocity saturated although OKN slow phase velocity continued to increase.4. The charge and discharge characteristics of OKAN were studied. The OKAN mechanism charged in 5-10 sec and discharged over 20-60 sec in darkness. The time constants of decay in OKAN slow phase velocity decreased as stimulus velocities increased. They also decreased on repeated testing. In several monkeys there was a consistent difference in the rate of decay of OKAN slow phase velocity to the right and left.5. Extended visual fixation discharged the activity responsible for producing OKAN. Short fixation times caused only a partial discharge of the OKAN mechanism. Following brief periods of fixation, OKAN resumed but with depressed slow phase velocities.6. A model based on a state realisation of a peak detector was formulated which approximately reproduces the salient characteristics of OKN and OKAN. This model predicts the three dominant characteristics of OKAN: (1) charge over 5-7 sec, (2) slow discharge in darkness, and (3) rapid discharge with visual fixation. With the addition of direct fast forward pathways, it also correctly predicts the rapid and slow rise in OKN. We postulate that OKAN is produced by a central integrator which is also active during OKN. Presumably this integrator acts to maximize velocities during OKN and to smooth and stabilize ocular following during movement of the visual surround.

Animals↗
PubMed1979

A comparison of duration of nystagmus as measured by the Southern California Postrotary Nystagmus Test and electronystagmography.

The Southern California Postrotary Nystagmus Test (SCPNT) and electronystagmography are methods used to evaluate one aspect of vestibular function. The SCPNT is based on the examiner's observation of eye movements and is used in combination with other information as part of a diagnostic battery for children with learning disorders. Electronystagmography is the permanent recording of eye movements through the use of surface electrodes. In this study. The SCPNT and an electronystagmograph were used to record postrotary nystagmus in 20 normal females aged 25 to 30. A significant correlation was found between the two tests for both duration and excursion. In addition, scores of both tests were compared for four normal and for four learning-disabled girls aged 7 to 8. The only significant correlation found was in terms of duration in the normal girls. Results were discussed in terms of factors affecting observation of eye movement, and differences between the nystagmus response of adults and children.

Adult↗
PubMed1979

The maturation of vestibular nystagmus in infancy and childhood.

The displacements, durations, and velocities of the slow and fast components of both the primary and secondary nystagmus induced by constant angular acceleration were measured in 46 normal children 1 month to 11 years old. There were significant changes in nystagmus parameters in respect to maturation. The young infant had larger amplitude, higher velocity beats than the older child during both the primary and the secondary nystagmus. Parameters describing both the primary and the secondary nystagmus reached their peak values and terminated earlier in the infant than in the older child. Although the slow component velocity during secondary nystagmus was much slower than during the primary nystagmus at all ages, the secondary nystagmus/primary nystagmus ratio was significantly greater in early infancy. Thus, in infancy, as compared with later childhood, the vigor of the secondary nystagmus was disproportionately greater than the primary nystagmus. These results were discussed in relation to the maturation both of vestibular responsiveness and of vestibular adaptation.

Age Factors↗
PubMedDate not supplied

Nystagmus alternans.

Alternating nystagmus is a spontaneous nystagmus which changes in direction without any external influence. In the literature this phenomenon has so far been described in 90 cases; in 12 of these, the nystagmus had a congenital origin. In contradistinction to the congenital type, the acquired type of alternating nystagmus is in most cases caused by a central nervous system disorder. We found the phenomenon of alternating nystagmus in 21 cases, in 15 of which it was congenital. The nystagmus was observed by means of electronystagmography. Differences were found between the two nystagmus types. The characteristics of alternating nystagmus are discussed.

Arnold-Chiari Malformation↗
PubMed1979

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 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.

Brain Stem↗
PubMed1979

[How useful is the intersaccadic interval analysis of vestibular nystagmus for clinical diagnostic (author's transl)].

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.

Caloric Tests↗
PubMed1979

Association between nystagmus hyporesponsivity and behavioral problems in learning-disabled children.

This study explored the hypothesis that an association exists between postrotary nystagmus hyporesponsivity and behavioral problems in learning-disabled children. Supporting this conclusion was the finding that the learning-disabled boys rated by teachers as displaying the most socially inappropriate behaviors had significantly lower postrotary nystagmus durations than other learning-disabled boys. In addition, near significant associations were obtained between subnormal nystagmus functioning and socially inappropriate responding for boys and girls combined. Learning-disabled girls were evaluated as responding significantly more appropriately than learning-disabled boys, while having significantly shorter postrotary nystagmus durations; thus, sex of a child may be an important variable in determining relationships between psychological characteristics and hyporesponsive nystagmus. Additional research is needed in this area because of a number of limitations to this study; however, these results present further suggestive evidence that learning-disabled children can be categorized according to characteristics of their postrotary nystagmus.

Child↗
PubMed1979

Jerk nystagmus: some new findings.

Eye movements in a subject with jerk nystagmus were recorded during a variety of tracking tasks using a photoelectric method. New findings included ability to reduce nystagmus amplitude and frequency when instructed "to hold the eye steady" rather than "to fixate" in the presence of a visible target, changes in nystagmus characteristics and visual acuity as a function of head position which related to overall retinal-image motion, marked variability of nystagmus especially during reading, and necessity of a prolonged period of visual feedback for generation of nystagmus to approach a "steady-state" level. Clinical implications of these findings are discussed, including use of the "hold" command during ophthalmoscopy in patients with nystagmus.

Adult↗
PubMed1979

Vestibular nuclei activity in the alert monkey during suppression of vestibular and optokinetic nystagmus.

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.

Animals↗
PubMed1979

Effect of ethacrynic acid upon the peripheral vestibular nystagmus.

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.

Action Potentials↗
PubMed1975

[Physiological spontaneous and positional nystagmus. electronystagmographic examinations concerning type, frequency and intensity (author's transl)].

120 subjects were selected from a large number of healthy persons on the grounds of their medical history and preexaminations including audiogram, which excluded the possibility of previous cochelo-vestibular illness. These 120 healthy persons were examined by means of electronystagmography. We were searching for spontaneous and positional nystagmus in 5 positions with open eyes in darkness and with closed eyes. 50% proved to have a horizontal and 82% a vertical spontaneous nystagmus in at least 1 position. The sex had no influence on the frequency and there was no difference in results under smokers and non-smokers. There was the same frequency of nystagmus directed to right and left. We conclude that there is a physiological horizontal spontaneous nystagmus of low intensity if fixation is completedly excluded. In our opinion it is not possible to determine a certain level of intensity above which a spontaneous nystagmus is pathological as the intensity of nystagmus is essentially dependent upon non-vestibular elements.

Dark Adaptation↗
PubMed1979

Latent, manifest latent, and congenital nystagmus.

Manifest latent nystagmus (MLN) was identified in 31 patients by accurate eye movement records. All the patients had horizontal tropias, and the nystagmus fast phases were always in the direction of viewing eye. The slow phases of MLN are decreasing-velocity exponentials while those of the jerk form of congenital nystagmus (CN) are increasing velocity exponentials. Several subjects who were believed to have latent nystagmus (LN) on clinical examination had small amplitude nystagmus evident by eye movement recording with both eyes open: these were actually cases of MLN. Many patients with MLN are misdiagnosed as having CN. An explanation for MLN and LN is provided based on confusion of egocentric directions between monocular and binocular viewing conditions.

Adolescent↗
PubMed1975

Vestibular nystagmus and teleost oculomotor neurons: functions of electrotonic coupling and dendritic impulse initiation.

1. Nystagmus in the horizontal plane is evoked in fish by mechanical stimulation of the ampulla of the horizontal semicircular canal or by electrical stimulation of the nerve from this canal. The movements are conjugate and the slow phase is away from the side of stimulation. 2. Medial rectus motoneurons were recorded from intracellularly, during nystagmus. During the slow phase (induced by ipsilateral stimulation), impulses arise abruptly from the base line and appear to arise at a distance from the cell body. During the fast phase (evoked by contralateral stimulation), impulses appear to arise from large PSPs that must be generated at or near the cell body. 3. In the curarized fish, stimulation of the nerve from the contralateral horizontal canal evokes spikes that arise from large EPSPs and that are blocked relatively easily by hyperpolarizing currents. Stimulation of the nerve from the ipsilateral horizontal canal evokes spikes that arise abruptly from the base line and that are much more difficult to block by hyperpolarizing currents. Little if any underlying PSP is observed when these impulses are delayed or blocked. Thus impulses evoked by stimulation of contralateral and ipsilateral side are initiated near to and far from the cell soma, respectively. 4. If impulses evoked by contralateral stimulation fail to excite the cell body due to injury, antidromic spikes are not occluded. Thus contralateral stimulation initiates impulses in the dendrites. 5. Cell bodies of neighboring motoneurons are coupled electrotonically, and graded antidromic stimulation evokes graded depolarizing potentials which result from electrotonic spread of spike activity from adjacent neurons. These depolarizing potentials are adequate to excite the cells in the presence of a background EPSP evoked by contralateral canal stimulation. In this manner coupling tends to synchronize cells during the fast phase of the nystagmus. 6. Antidromic responses of neighboring cells fail to interact with dendritic inputs to a particular cell, although indirect evidence indicates antidromic spikes invade the impulse-initiating regions in the dendrites. Thus coupling between dendrites is negligible and dendritic inputs can mediate the smoothly graded movements of the slow nystagmic phase. Coupling between somata is too weak to cause significant interaction between dendritically evoked impulses (unless the cell bodies are depolarized by EPSPs). 7. Rhythmic firing can be recorded in a single presynaptic fiber corresponding to either the slow or the fast phase of nystagmus, but not to both. Oculomotor neurons appear to be "relay cells" that, during the fast phase of the nystagmus receive a synchronized synaptic input which is initiated in a higher level command nucleus.

Animals↗