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At least 19 recordsLinked to original sources
PubMed1983

The nystagmus blockage syndrome. Congenital nystagmus, manifest latent nystagmus, or both?

We have carefully studied, by quantitative oculography, a patient with the nystagmus blockage syndrome (NBS), and two patients with a similar disorder of eye movements that might be mistaken clinically for NBS. Our recordings revealed two distinctly different abnormalities present in a single patient with NBS. Our NBS patient exhibited congenital nystagmus (CN) waveforms when viewing at distance; the CN did not damp with convergence on a near target. When the patient allowed one eye to become esotropic, however, the nystagmus damped considerably and abruptly changed from CN to manifest latent nystagmus (MLN). This peculiar transition from CN to MLN has not been described previously. The appearance of MLN in a case with ongoing CN suggests that two different mechanisms may underlie NBS, since the only other case documented with eye movement recordings showed no transition to MLN. Because the diagnosis of NBS usually is made on evidence of clinical signs alone, it is probable that these two types have been combined indiscriminately and presented as one syndrome. In addition, our discovery of two mechanisms discernable only by quantitative recording suggests that NBS has been diagnosed inappropriately in patients with clinically similar but oculographically different eye signs. Further quantitative studies are required to fully define NBS and to determine if these are the only two mechanisms found in this syndrome.

Adolescent↗
PubMed1998

Relationships among visual acuity demands, convergence, and nystagmus in patients with manifest/latent nystagmus.

BACKGROUND: We investigated the role convergence plays in nystagmus dampening, in particular, relationships among visual acuity demands, convergence, and nystagmus. Previously we showed that subjects with idiopathic infantile nystagmus exhibit a range of responses to acuity targets, one of which is nystagmus blockage syndrome. We report herein eye movement responses to acuity targets of patients with manifest/latent nystagmus. METHODS: Fourteen patients, 11 with latent or manifest latent nystagmus and 3 with combined manifest latent with infantile nystagmus, were asked to indicate the direction of the gap in Landolt C optotypes while their eye movements were recorded. RESULTS: The tested patients exhibited various responses to acuity demands: (1) dampening of nystagmus with convergence (i.e., nystagmus blockage syndrome) (5/14 patients), (2) changes in vergence without nystagmus dampening (2 patients), (3) decrease of nystagmus without convergence (2 patients), and (4) little change in nystagmus or vergence (5 patients). In nystagmus blockage syndrome the amount of convergence increased with acuity demands in two of five patients and the convergence duration in four of five patients; nystagmus dampening increased with acuity demands in one of five patients and the blockage duration in four of five patients. CONCLUSIONS: Many, but not all, patients with manifest/latent nystagmus, similar to those with infantile nystagmus, used convergence to dampen their nystagmus. The convergence response tended to increase with acuity demands, but the amount of dampening was idiosyncratic and not predictably related to the measured convergence across patients.

Adolescent↗
PubMed1992

[The vertical component in a caloric nystagmus and the existence of a second phase of the nystagmus--the possibility of canal otolithic interaction in normal subjects].

To clarify the existence of the vertical component during a caloric nystagmus and the existence of a second phase of the nystagmus, 194 induced incidents of a caloric nystagmus in 29 normal subjects have been analyzed. Each nystagmus episode was recorded by using ENG and an infra-red video camera. The caloric stimuli were given by pouring 5 ml of water at 20 degrees C into the ear at an ear-up position. After irrigation, each subject then assumed a supine or a prone position, with the head bent 30 degrees forward in either position. All recordings contained vertical components that depended on the supine or prone head position and not on the side of the stimulated ear, i.e., an up-beating nystagmus resulted in the supine position and a down-beating nystagmus in the prone position. Further, the vertical component was far stronger in the prone position. In contrast, the horizontal component had larger velocities and was of longer duration in the supine position than in the prone position. When the first phase of the caloric nystagmus ended, the body position was changed 90 degrees, i.e., to a sitting position or a right-ear-down or left-ear-down position. All trials showed a horizontal component during the secondary phase when the head assumed the sitting position. As for the ear-down positions, only when the irrigated ear was moved upwards from the prone position during the secondary phase, an up-beating vertical nystagmus resulted in almost all the trials. These findings suggest that a caloric nystagmus may originate not only from the lateral semicircular canal but also from the vertical canals, and the second phase of a caloric nystagmus may be strongly influenced by the otolithic organs.

Electronystagmography↗
PubMed1984

Vertical optokinetic nystagmus and vestibular nystagmus in the monkey: up-down asymmetry and effects of gravity.

Vertical optokinetic nystagmus (OKN) i.e., OKN in the sagittal plane, was asymmetrical in the monkey when it was induced with animals lying on their sides in a 90 degrees roll position. In typical monkeys the slow phase velocity of downward OKN (slow phases up) increased proportionally with stimulus velocity at close to unity gain to about 60 degrees/s and saturated at about 100 degrees/s. Upward OKN (slow phases down) increased with close to unity gain only to about 40 degrees/s and saturated at about 60 degrees/s. The slow phase velocity of upward OKN was usually irregular and its frequency was lower than that of downward or horizontal OKN. Upward and downward optokinetic after-nystagmus (OKAN) were also asymmetrical. Upward OKAN was weak or absent and when present it usually saturated at 10 degrees/s. Downward OKAN was stronger, increasing with a gain of about 0.7 with regard to stimulus velocity to a saturation velocity of about 50-60 degrees/s. This was usually about 10-30 degrees/s less than the saturation velocity of horizontal OKAN. The weak or absent upward OKAN indicates that stored activity related to slow phase eye velocity contributes little to the production of upward OKN. In agreement with this, there was little or no slow rise in slow phase velocity to a steady state level during upward OKN. Instead eye velocity rose to its peak velocity at the onset of stimulation. The lack of stored velocity information is probably largely responsible for the differences in regularity, gain and frequency between upward and downward OKN. Vertical vestibular nystagmus was induced by rotating monkeys in darkness with steps of velocity about a vertical axis, while they were lying on their sides in a 90 degree roll position. The velocities of the initial upward and downward slow phases were approximately equal. Gains of the vertical VOR ranged from about 0.5 to 0.98 for stimuli up to 150 degrees/s. Despite equivalent initial gains for upward and downward nystagmus, the vertical VOR was asymmetrical in that downward nystagmus had a higher frequency and generally lasted longer than upward nystagmus. Time constants of downward nystagmus (slow phases up) were about 15 s on average and were similar to those of horizontal nystagmus. Mean time constants of upward nystagmus (slow phases down) were about 8 s. This is only slightly longer than the average time constant of afferent activity in the semicircular canal nerves induced by steps of velocity.(ABSTRACT TRUNCATED AT 400 WORDS)

Acoustic Stimulation↗
PubMedDate not supplied

What can acquired nystagmus tell us about congenital forms of nystagmus?

For several forms of acquired nystagmus, animal models exist, mathematical hypotheses have been proposed, and treatments are available. What insights could acquired nystagmus provide for congenital forms of nystagmus? Acquired periodic alternating nystagmus (PAN) is caused by instability of the velocity storage mechanism for vestibular eye movements; an adaptive mechanism produces the oscillations that have a period of about 4 minutes. Surprisingly, the ability of individuals with congenital forms of nystagmus to adapt their eye movements to new visual demands has received little study. Acquired pendular nystagmus (APN) may arise from instability in the neural integrator for eye movements; identification of the neurotransmitters contributing to normal gaze holding made it possible to identify candidate drugs for treatment of APN. Similar knowledge of the biology underlying of congenital forms of nystagmus might similarly suggest effective drugs. Downbeat nystagmus (DBN) is caused by cerebellar disease, which includes structural lesions affecting the flocculus and paraflocculus, and calcium channelopathies, such as episodic ataxia type 2 (EA2), for which a mouse model and effective treatment is available. Since some congenital forms of nystagmus are genetic in origin, then the possibility arises that they may be caused by a channelopathy, a hypothesis that suggests novel drugs for evaluation in randomized controlled trials.

Animals↗
PubMed1983

Primary position upbeating nystagmus. A variety of central positional nystagmus.

We report a collaborative study of 11 patients with upbeat nystagmus in the primary position of gaze. In most cases the nystagmus behaved in accordance with Alexander's Law; in 3 patients convergence enhanced the nystagmus. Lateral gaze was without effect in 7 instances. Static tilt to prone and supine positions altered the characteristics of the nystagmus in 7 patients. The effects were variable and, in one case, there was reversal of the direction of the nystagmus to downbeating. There was pathological or radiological confirmation of lesions in the pontomedullary junction (2 cases) and the pontomesencephalic junction (2 cases). The findings support previous reports that primary position upbeat nystagmus occurs predominately with intra-axial brainstem lesions. There is one report of its occurrence with an intrinsic cerebellar lesion. Modification of the amplitude of upbeat nystagmus by tilt of the head with respect to gravity in the majority of patients implies an otolith-related component in the genesis of the nystagmus.

Adult↗
PubMed2003

Latent nystagmus and acquired pendular nystagmus masquerading as spasmus nutans.

SUMMARY: We used ocular motility recordings to identify the characteristics of a rare combination of conjugate, horizontal jerk, and pendular nystagmus in a 9-year-old boy. The clinical diagnoses were amblyopia, left esotropia, congenital nystagmus, and an apparently uniocular pendular nystagmus that mimicked spasmus nutans. Ocular motility recordings revealed an unusual latent/manifest latent nystagmus, pendular nystagmus with characteristics of an acquired nystagmus, and uniocular saccades. The ocular motor data identified clinically unrecognized types of nystagmus and suggested that the pendular nystagmus was acquired in infancy rather than as a result of failure to develop good vision or binocularity. The presence of uniocular saccades adds to the mounting evidence that individual control for each eye exists in humans.

Child↗
PubMed1984

Role of the central and peripheral retina upon optokinetic nystagmus. Foveal and peripheral nystagmus.

The optokinetic (OK) nystagmus induced by OK stimulus on the foveal area (foveal nystagmus) or on the peripheral retina (peripheral nystagmus) are discussed. Separation of the visual field can be achieved by a combination of a projection type OK stimulator and a masking cylinder driven by a d.c. ENG. Foveal and peripheral nystagmus became increasingly difficult to elicit in tact with narrowing of the visual field or increase in stimulus velocity. The influence of velocity was much more noticeable in the foveal nystagmus. The characteristics of foveal and peripheral OK nystagmus are elucidated by the overlapping method. The foveal nystagmus has a rather distorted form, but its slow-phase eye velocity is the same as the target velocity. It has a tendency to start and reverse with slow phase. Its beating field deviates in the direction of the slow phase. The peripheral nystagmus, on the contrary, has a typical saw-tooth form and its slow-phase eye velocity is slower than the target velocity, even at the low speed stimulus. It has a tendency to start and reverse with the quick phase. Its beating field deviates in the direction of the quick phase.

Eye Movements↗