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

Current models of the ocular motor system are usually presented in their most reduced form, are unilateral in architecture, and precise yoking is presumed. Although this simplifies the models, it does not accurately simulate the actual neuroanatomy and limits the models to simple, stereotyped responses. Studies of normal humans and monkeys have demonstrated striking disconjugacies in normal responses. Normal saccades may be disconjugate, or 1 eye may exhibit a dynamic overshoot. Asymmetric vergence can result in disconjugate saccades, unequal magnification spectacles cause differential saccadic gain adjustment, and saccades to unequal disparities also cause unequal saccades in the 2 eyes. In strabismus, deviated eyes typically do not mimic the movements of the fixating eye nor do their latent or congenital nystagmus waveforms duplicate those of the fixating eye. In spasmus nutans, each eye oscillates independently of the other. In achiasmatic dogs, uni-ocular saccades and uni-ocular nystagmus waveforms are seen; the same may be true in human achiasma. These data from both normals and those with abnormalities suggest that current models for ocular motor control are inadequate representations of the actual system. The inability of unilateral, yoked control (or even bilateral, yoked control) system models to duplicate the ocular motor responses of binocular mammals suggests that their ocular motor systems evolved from the bilateral, independent control systems seen in chameleons. One need only postulate a yoking overlay superimposed on two independent control systems to achieve conjugacy (bilateral, yoked, independent control) of the eyes. Abnormalities producing grossly disconjugate eye movements may then be simulated using the independent control of each eye released by a deficiency in the yoking overlay. Independent control of each eye coupled with the essential bilateral brain stem architecture implies that each individual muscle is driven by independent populations of neurons (burst cells, neural integrator cells, etc.). The agonist muscles of each eye are usually coordinated (yoked) but may function independently if the task dictates or if binocularity did not develop. Models based on the above architecture would be robust and could duplicate the many responses (both normal and abnormal) possible from the neurophysiological system.
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PMID:Evidence suggesting individual ocular motor control of each eye (muscle). 799 79

The authors examined five young children with monocular vision loss who developed monocular nystagmus. The nystagmus was of fast frequency and small amplitude in all fields of gaze. In four children, successful treatment of the cause of the vision loss resulted in cessation of the nystagmus. No child showed signs of spasmus nutans, or of optic nerve or chiasmal tumor. The evaluation of the young child with unilateral nystagmus should begin with a careful eye examination.
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PMID:Monocular nystagmus caused by unilateral anterior visual-pathway disease. 825 90

Two children with congenital stationary night blindness were originally diagnosed as having spasmus nutans. Both children had the typical features of spasmus nutans including asymmetric nystagmus, head shaking, and torticollis. The diagnosis of congenital stationary night blindness was established only after each child underwent electroretinography. The nystagmus associated with retinal disease can mimic many of the features of spasmus nutans. Children suspected of having spasmus nutans should undergo complete ophthalmologic examination and electroretinography if they are myopic.
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PMID:Retinal disease masquerading as spasmus nutans. 835 Oct 22

A small number of children who develop disconjugate nystagmus, torticollis, and head titubation (spasmus nutans) have been found to have optic chiasm or third ventricle gliomas. However, the prevalence of glioma or other developmental abnormalities in this disorder is unknown because no large series of spasmus nutans cases has previously been reported. A reviewer of the records of 67 consecutive children initially diagnosed with spasmus nutans and followed for an average of 3.3 years at the St Louis Children's Hospital revealed the following: 61% had a history of prematurity, developmental delay, or other systemic abnormality; strabismus, most commonly infantile esotropia, developed in 55%; 43% had neuroimaging studies; and 0% had evidence of a glioma or showed signs of tumor on follow-up examinations. From this consecutive patient series, we estimate the prevalence of tumor in spasmus nutans to be less than 1.4%. Without other evidence of an intracranial mass lesion, neuroimaging of infants initially diagnosed with spasmus nutans may not be immediately warranted.
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PMID:Prevalence of intracranial lesions in children initially diagnosed with disconjugate nystagmus (spasmus nutans) 896 30

Spasmus nutans is classically described as a triad of nystagmus, head nodding and torticollis. It occurs in children, beginning in infancy and usually disappears in childhood. It is uncommon but its prompt recognition by ophthalmologists, paediatricians and neurologists can provide reassurance to the family of its benign nature. It is important to distinguish it from more serious conditions like gliomas which may present with signs mimicking spasmus nutans. We describe a case of a 3-year-old boy with acquired horizontal pendular nystagmus associated with head nodding and torticollis. The diagnosis of spasmus nutans, its implications and its management are discussed.
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PMID:Spasmus nutans. 889 38

Horizontal asymmetric nystagmus usually occurs in one of three situations: secondary to an intracranial lesion, with monocular visual loss, or as part of the triad that constitutes the diagnosis of spasmus nutans (asymmetric nystagmus, abnormal head posture, head shake). Clinical records of 277 children, presenting with congenital nystagmus over an 8-year period were reviewed. Nystagmus was asymmetric in 24 of 277 cases. Seven of these patients were diagnosed with spasmus nutans. This is a rare condition that is only diagnosed retrospectively based on the absence of any abnormal neuroimaging or electrophysiological findings. Twelve of 24 patients had intracranial pathology and all had abnormal visual evoked potentials (VEPs). Five patients were diagnosed with congenital sensory defect nystagmus including one with albinism, three with congenital cone dysfunction, and one with cone-rod dystrophy. This paper stresses that although neuroimaging is necessary in all patients presenting with asymmetric nystagmus, such nystagmus can also occur with retinal disease or albinism and indicates the importance of non-invasive VEP/ERG testing in all forms of nystagmus.
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PMID:Diagnosing children presenting with asymmetric pendular nystagmus. 1157 Jun 32

Congenital and acquired nystagmus, particularly pendular and jerk nystagmus, see-saw nystagmus and spasmus nutans, may be the presenting sign of a suprasellar mass lesion.(1) The large variety of different suprasellar mass lesions requiring quite different therapeutic measures necessitates exact histological diagnosis for optimal therapeutic strategy planning.(2) Stereotactic tumor biopsy has become a well-established diagnostic approach, combining minimal surgical trauma with a high degree of diagnostic safety. Particularly in the two most frequent suprasellar mass lesions - craniopharyngiomas and pilocytic astrocytomas - accurately planned stereotactic drainage of tumor cysts combined with radiotherapy and/or stereotactic radiosurgery allows successful decompression and tumor control as well as maximum preservation of visual and endocrinological functions when compared with conventional surgical procedures.(2-11)
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PMID:Nystagmus in suprasellar tumors: recent advances in diagnosis and therapy. 1222 98

The aim of this study was to characterize children with transient nystagmus. Eleven children (six males, five females) developed nystagmus in infancy and then experienced regression of the problem, usually within a few months. Mean age at onset was 2.7 months, and mean age at regression was 8.5 months. No etiology could be ascertained in any of the patients, although four children had other eye or vision abnormalities (regressed retinopathy of prematurity, n=1; asymmetric fundus colobomata, n=1; delayed visual maturation, n=2). Results of this study suggest that mechanisms which allow ocular motor stability undergo a period of postnatal maturation, during which nystagmus can occur, but also during which nystagmus may disappear. Not every case of transient nystagmus should be categorized as spasmus nutans. There is a subset of infants and young children who develop transient nystagmus with no other findings and in whom the nystagmus disappears.
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PMID:Transient, idiopathic nystagmus in infants. 1272 43

The Heimann-Bielschowsky phenomenon (HBP) refers to coarse vertical oscillation of the eye with impaired vision. The ocular movements are strictly monocular, occurring only in the eye with amblyopia. The vertical oscillation is of equal velocity in both vertical directions, or may sometimes be greater in the downward than upward direction. HBP develops several years after loss of vision. It can be differentiated from dissociated nystagmus in spasmus nutans, congenital nystagmus and internuclear ophthalmoplegia based on the strict unilaterality, vertical direction and low frequency. Previously, only a few reports described the development of oscillopsia due to HBP after cataract surgery, which resolved spontaneously or responded to gabapentin. However, visual impairments due to diplopia or oscillopsia from HBP after cataract surgery have received little attention. We report a man who developed persistent vertical diplopia and oscillopsia due to HBP after a cataract operation, which markedly impaired his vision.
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PMID:Emergence of diplopia and oscillopsia due to Heimann-Bielschowsky phenomenon after cataract surgery. 1881 21

Nystagmus is an involuntary, periodic eye movement caused by a slow drift of fixation which is followed by a fast refixation saccade (jerk nystagmus) or a slow movement back to fixation (pendular nystagmus). In childhood most cases are benign forms of nystagmus: idiopathic infantile, ocular or latent nystagmus. They arise at the age of 3 months, without oscillopsia and show the absence of the physiologic opto-kinetic nystagmus. A full ophthalmologic evaluation is all that is needed in most cases: albinism, macular or optic nerve hypoplasia and congenital retinal dystrophies are the most common forms of ocular nystagmus. Idiopathic infantile nystagmus can be hereditary, the most common and best analyzed form being a mutation of the FRMD7 gene on chromosome Xq26.2. The mutation shows a mild genotype-phenotype correlation. In all female carriers the opto-kinetic nystagmus is absent and half had mild nystagmus. Latent nystagmus is part of the infantile esotropia syndrome and shows the unique feature of change of direction when the fixing eye changes: it is always beating to the side of the fixing eye. There is no cure for infantile nystagmus but therapeutic options include magnifying visual aids or eye muscle surgery at the age of 6-8 y in patients with head turn. Less than 20% of childhood nystagmus are acquired and need further neurological and imaging work-up. Alarming signs and symptoms are: onset after the age of 4 months, oscillopsia, dissociated (asymmetric) nystagmus, preserved opto-kinetic nystagmus, afferent pupillary defect, papilloedema and neurological symptoms like vertigo and nausea. The most common cause is due to pathology of the anterior optic pathway (e.g. optic nerve gliomas). It shows the same clinical feature of dissociated nystagmus as spasmus nutans but has a higher frequency as in INO. Other forms of acquired nystagmus are due to brainstem, cerebellar or metabolic diseases.
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PMID:Infantile and acquired nystagmus in childhood. 2245 7


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