Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Nystagmus, Pathologic”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the 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
PubMed1985

[Pathologic nystagmus and related phenomena. A review].

Pathological nystagmus may be spontaneous, positional, or gaze-evoked. Peripheral vestibular nystagmus is usually rotatory, the horizontal component being most prominent. It is - in contrast to a central vestibular nystagmus - strongly inhibited by fixation. Spontaneous congenital nystagmus is also prominent with fixation, but it can usually be distinguished from acquired fixation nystagmus based on its long duration, atypical waveforms and high frequency. Two general types of positional nystagmus can be identified on the basis of nystagmus regularity: static and paroxysmal. The most common variety of positional nystagmus is the so-called benign paroxysmal positional nystagmus, which in the majority of cases occurs as an isolated symptom of unknown cause. Gaze-evoked nystagmus, prominent with fixation, includes dissociated, rebound and gaze-paretic nystagmus forms. Symmetrical gaze-evoked nystagmus is most commonly produced by ingestion of certain drugs. Phenomena related to nystagmus include: amblyopic, voluntary, and convergence-retraction nystagmus, ocular dysmetria, ocular flutter, opsoclonus, ocular bobbing, and ocular myoclonus.

Amblyopia↗
PubMed1976

Pathologic nystagmus: a classification based on electro-oculographic recordings.

The widespread availability of eye movement recording systems has added a new dimension to our ability to accurately describe nystagmus. Electrooculography (EOG) is the simplest and most readily available system. With EOG the effect of loss of fixation (either with eyes closed, or eyes open in darkness) can be accurately assessed and quantitative evaluation of nystagmus speed, frequency and amplitude is easily made. Of equal importance, it provides a permanent record that can be compared with nystagmus recorded in other patients. By comparing clinical observation with paper recordings, both students and experienced clinicians can become more efficient in recognizing different varieties of nystagmus.

Electrooculography↗
PubMed1996

Positional nystagmus in asymptomatic human subjects.

Nystagmus produced by static placement of the head in different orientations is termed positional nystagmus and is known to occur in human subjects who are free of vestibular symptoms. This study provides quantitative data for horizontal positional nystagmus occurrence in 49 normal human subjects, in whom the number of nystagmus beats, the slow-phase velocity of each beat, and distribution statistics were determined. A metric for the possible differentiation of physiologic positional nystagmus from pathologic nystagmus is described.

Diagnosis, Differential↗
PubMed1994

Treatment of abnormal eye movements that impair vision: strategies based on current concepts of physiology and pharmacology.

Certain abnormal eye movements, especially pathological nystagmus, degrade vision and cause illusory motion of the seen environment. These symptoms are due to excessive movement of images of stationary objects on the retina. Recently, the pathophysiology underlying several types of nystagmus and saccadic oscillations was better defined by the development of animal models and by experimental pharmacological studies. Despite this, few reliable therapies are currently available for these abnormal eye movements. In clinical studies, a number of drugs reportedly helped individual patients, but few drugs have been subjected to double-blind trials. An alternative approach to pharmacological suppression of abnormal eye movements is optical stabilization of images on the retina, which is helpful in selected patients. Weakening of the extraocular muscles, using botulinum toxin or surgery, is prone to cause diplopia and may induce plastic-adaptive changes that render the effect temporary. In some patients, treatment of an underlying condition, such as the Arnold-Chiari malformation, reduces nystagmus and improves vision. There is a need for multicenter trials to evaluate systematically potential treatments of abnormal eye movements that impair vision.

Animals↗
PubMed2005

How the eyes move the body.

The increased postural sway of patients with disorders of the vestibular system improves with vision. The suppression of pathologic nystagmus also reduces sway. Because the latter effect cannot be attributed to retinal slip as a relevant feedback for postural control, the authors investigated how eye movements rather than retinal slip affect balance. They found that slow eye movements increase sway, possibly by an efference copy, which explains why spontaneous nystagmus causes postural imbalance.

Adult↗
PubMed1982

Is spontaneous nystagmus a pathological sign?

This study was undertaken to determine the incidence of spontaneous nystagmus (SN) in normals and evaluate its significance in patients. There were 60 normal subjects and SN was recorded in 8 (13%). Between January 1979 and November 1981, SN without past pointing was the only detectable abnormality in 41 patients undergoing a vestibular evaluation. An intracranial lesion could be confirmed in 34 patients (83%). There results from both normal subjects and patients are compared with earlier reports in the literature. Because of differences in nomenclature and classification of SN and differences in technique of searching and recording SN, no true comparisons are possible. Our conclusion is that SN in normals should be regarded as an oculomotor abnormality for which there is no detectable cause. In patients SN is a valuable diagnostic sign and should be considered significant regardless of its slow phase velocity.

Adolescent↗
PubMed1983

[Cervical nystagmus caused by proprioceptors of the neck].

A pathological nystagmus, occurring during turning of the trunk in relation to the head, which is held stationary in space, clearly points towards a cervical origin of vestibular vertigo. Such a cervical nystagmus may have a vascular origin by the compression of the arteriae vertebrales, or a proprioreceptive origin via the upper neck joints, or it may possibly be due to functional disturbances of the upper cervical spine. The dynamic characteristics of the so-called cervico-ocular reflex can be examined only in patients with non-functioning labyrinths, since in a healthy person the reflex is so strongly suppressed that it cannot be analyzed any more. In five patients with isolated bilateral complete vestibular deficiencies, we found a strong cervico-ocular reflex. Detailed examinations showed that nystagmus occurred during turning of the body in relation to the head ("phasic neck reflex"). On the other hand, when remaining in the extreme positions, the proprioreceptive nystagmus does not persist. Contrary to this, a cervical nystagmus due to vascular causes shows a latency period after torsion of the neck and increases if the head remains in the extreme position. Before assuming a cervical origin of a vestibular vertigo, an examination for cervical nystagmus should be carried out. Such a cervical nystagmus is the only definite pointer towards a relation between an upper cervical spine syndrome and vertigo, which is sometimes assumed rather uncritically.

Adult↗
PubMed2000

Vestibular dysfunction in Gulf War syndrome.

METHODS: Vestibular complaints of Gulf War veterans were characterized by a nested case-control study of 23 veterans with 3 different Gulf War syndromes and 20 matched control subjects. All subjects completed a standardized symptom questionnaire and underwent standard audiovestibular tests administered by audiologists blinded to group identities. RESULTS: The prevalence of reported dizzy spells was higher in veterans with Gulf War syndromes 1 (100%), 2 (85%), and 3 (100%) than in controls (25%, P < 0.0001). Dizzy spells were more frequent, lasted longer, and involved a wider variety of accompanying symptoms in veterans with syndrome 2 than in those with syndromes 1 and 3. Audiovestibular testing showed greater interocular asymmetry of nystagmic velocity on sinusoidal harmonic acceleration in syndromes 1 (P = 0.015) and 2 (P = 0.002), greater asymmetry of saccadic velocity in syndrome 2 (P = 0.4), diminished nystagmic velocity after caloric stimulation bilaterally in syndrome 3 (P = 0.02 to 0.04), more subjects with pathologic nystagmus (P = 0. 09), and greater interside asymmetry of wave I to III interpeak latency on auditory brain stem response in syndromes 1 (P = 0.005) and 2 (P = 0.07). Asymmetry of gain on sinusoidal harmonic acceleration and pathologic nystagmus were most strongly associated with symptoms of paroxysmal vertigo (P = 0.002 and 0.07, respectively); asymmetry of saccadic velocity, with the severity of vertigo (P = 0.004); and abnormal caloric response, with chronic dysequilibrium (P = 0.006). CONCLUSIONS: The findings are compatible with a subtle neurologic injury from organophosphate-induced delayed neurotoxicity.

Adult↗
PubMed1999

Diagnostic criteria for central versus peripheral positioning nystagmus and vertigo: a review.

Head positioning can lead to pathological nystagmus and vertigo. In most instances the cause is a peripheral vestibular disorder, as in benign paroxysmal positioning vertigo (BPPV). Central lesions can lead to positional nystagmus (central PN) or to paroxysmal positioning nystagmus and vertigo (central PPV). Lesions in central PPV are often found dorsolateral to the fourth ventricle or in the dorsal vermis. This localization, together with other clinical features (associated cerebellar and oculomotor signs), generally allows one to easily distinguish central PPV from BPPV. However, in individual cases this may prove difficult, since the two syndromes share many features. Even if only BPPV as a peripheral lesion is considered, differentiation based on such features as latency, course, and duration of nystagmus during an attack, fatigability, vertigo, vomiting, and time period during which nystagmus bouts occur, may be impossible. Only the direction of nystagmus during an attack can allow differentiation.

Diagnosis, Differential↗
PubMed2000

Nystagmus.

This report reviews the recent contributions to the field of pathologic nystagmus. The classification and nomenclature of nystagmus with onset in infancy is controversial. Because there are differences in nystagmus forms between patients with idiopathic nystagmus and those with nystagmus associated with afferent sensory defects, a distinction between these two nystagmus types is proposed. The distinctions are also helpful for clinicians, because these separate entities imply different diagnostic evaluations and visual prognosis. Recent studies have confirmed that periodic alternating nystagmus is detected more easily if the patient is evaluated for a longer time period and occurs more commonly than previously thought. Psychophysical investigations indicate that extraretinal signals play an important role in suppression of oscillopsia in infantile nystagmus. Genetic analysis recently has allowed identification of genes of X-linked idiopathic nystagmus and achromatopsia.

Evoked Potentials, Visual↗