Nystagmus

In the last ten to fifteen years refinements in the registration techniques for ocular movements have allowed a more precise definition of nystagmus forms and have thus brought new insight into their pathophysiology. As a result we can distinguish four types of disturbances of the subsystem for the slow movements, which are fundamental to nystagmus. This and other discoveries also have consequences for the practical diagnostics of neuro-ophthalmological diseases. In this article, with the help of a simple practical scheme extra attention will be given to the clinically relevant new information needed to make the diagnosis or differential diagnosis of conditions in which nystagmus is one of the most important signs.     

Nystagmus

Patients who present with nystagmus may have visual loss, a benign peripheral vestibular abnormality, or an important central nervous system disorder. The clinical history, features of nystagmus on examination, and accompanying symptoms and findings often help to localize the lesion. These features also determine the appropriate evaluation and treatment of the underlying disorder. Additionally, if there is oscillopsia or blurred vision, treatment of the nystagmus itself may be warranted. Possible treatments include medication, optical manipulations, and surgery.     

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.     

Nystagmus

Acquired nystagmus causes excessive motion of images on the retina, which often reduces visual acuity and produces oscillopsia (illusory motion of the seen world). The pathogenesis of several forms of acquired nystagmus is now better understood and can be related to abnormalities of mechanisms that normally hold gaze steady. Basic research on the pharmacology of the neural pathways responsible for gaze holding has demonstrated an important role for gamma aminobutyric acid and led to new drug treatments for acquired nystagmus and its visual consequences.     

Nystagmus

Electronystagmographic studies with an attempt to quantify various parameters of congenital nystagmus are interesting although not conclusive clinically. This is due to the spontaneous variability of congenital nystagmus. A qualitative study (position and velocity) may be sufficient for clinical examination and treatment of congenital nystagmus. The quantification of the optokinetic response is also clinically difficult. This comes from the fact that various factors can affect the response; even healthy patients can have variable gain. However the optokinetic test, which compares the response to a nasotemporal and temporonasal stimulation, is useful. It enables us to identify patients who never had a visual binocular experience in their first year of life and who keep a directional asymmetry of the monocular optokinetic response.     

Nystagmus

This article presents an overview of the pathophysiology of nystagmus and the differential diagnostics of congenital and acquired nystagmus. In addition, the principles of conservative, surgical and pharmacotherapy treatment options are described. The pathophysiological basis of nystagmus deepens the understanding of the etiology of the individual forms of nystagmus. The therapeutic approach to calming of nystagmus aims at an extension of the foveation time, which has the most significant impact on visual acuity. In congenital nystagmus this can be carried out by optimization of the retinal image, prisms or by bilateral surgical muscle repositioning to use the phenomenon of a null or neutral zone. In acquired nystagmus the off-label use of centrally acting medications can sometimes be helpful to calm the nystagmus and the associated oscillopsia.     

Nystagmus

Nystagmus continues to be a complex subject of study. Our ability to characterize nystagmus has improved, but our comprehension of the oculomotor control process underlying this condition remains vague. We review recent advances in the characterization, classification, and treatment of nystagmus. Congenital forms of nystagmus, nystagmus associated with strabismus, and available therapeutic options for congenital and acquired nystagmus are emphasized.     

Nystagmus

This article reviews the recent literature on nystagmus and various aspects of the pathophysiology of congenital idiopathic nystagmus and nystagmus treatment. One paper shows a new classification of latent/manifest latent nystagmus based on eye movement recordings. Nystagmus associated with complex syndromes and with onset in childhood represents the subject of several important recent articles, as does acquired nystagmus. Nystagmus as a manifestation of the toxicity of pharmacological agents is becoming increasingly recognized. Important contributions have been made to the genetics of various forms of nystagmus that represent an essential feature of retinal diseases, such as congenital stationary night blindness, albinism, blue cone monochromatism, and achromatopsia.     

Nystagmus.

This article reviews some of the past year's important papers, with emphasis on early onset and acquired neurological nystagmus. Advances in understanding the mechanisms of suppression of oscillopsia, the evolution of nystagmus, and the treatment of periodic alternating nystagmus and of nystagmus in albinism have been made in early-onset nystagmus. Successful pharmacological treatment for acquired neurological nystagmus has been demonstrated with the gamma aminobutyric acid agonist gabapentin and with memantine, a glutamate antagonist.