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Query: UMLS:C0038379 (strabismus)
 9,317 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The principle of Kestenbaum's surgical rotation of the eyes has been found applicable to cases with head tilt to the shoulder. With restriction to the anterior parts of the obliques, which are acting mainly rotatory, the authors were able to release 9 patients out of 25 from their abnormal head posture with their operation. 12 showed definite improvement. However, the pathophysiology and the abolition of the head tilt to the shoulder could not alltogether be explained yet. Latent nystagmus with a resting position is found in only two out of three, a rotatory component only in one out of three patients. The authors believe that the picture of head tilt to the shoulder may rather be located within the classification of congenital strabismus syndrome (Lang) than within a strict causal classification after a certain type of nystagmus.
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PMID:["Kestenbaum's surgical rotation of the eyes" in patients with head tipped to the shoulder (author's transl)]. 73 85

We report eye movement findings in 30 patients with latent nystagmus and who were found to have a variety of associated oculomotor disorders. Latent nystagmus is defined clinically as nystagmus which appears on covering one eye and beats towards the uncovered eye. Recordings showed that the latent nystagmus in 28 patients had slow phases with linear or exponentially decreasing velocity. This nystagmus is termed 'LN'. In 13 of these patients certain manoeuvres (e.g. pursuit) provoked nystagmus with exponentially increasing slow phase velocities characteristic of the congenital form of nystagmus termed 'CN' and we propose that this is a forme fruste of CN. In two patients the nystagmus provoked by cover was latent CN. Twenty-nine patients had a history of strabismus and one had a marked phoria. Some patients had amblyopia whilst others had normal vision in each eye. Although binocular vision was usually absent, six patients had varying degrees of stereopsis. A temporonasal predominance of monocularly elicited optokinetic response previously associated with LN, was present only in a minority of patients. Some responses were bidirectionally absent or of low velocity, possibly the result of a cortical impairment of visual motion detection. The most deranged responses had slow phases which were in the opposite direction to the stimulus as described in CN. The presence of 'forme fruste' CN in many of these patients suggests that some of the derangements of optokinetic responses are due to CN. The findings indicate a greater overlap between the incidences of LN and CN than previously estimated. Thirty percent of patients had large saccadic 'square wave' intrusions. These were not present when there was marked amblyopia. They are attributed to a competitive incongruence of visual fields and eye positions. Dissociations found between the presence and severity of strabismus, stereopsis, amblyopia and optokinetic abnormalities point to these features being relatively independent although associated in typical clusterings. This is evidence against the theory that strabismus and LN are directly caused by nasotemporal optokinetic imbalance which persists because of failure to develop binocular vision. The variability of findings favours the view that LN and CN arise from a genetic or acquired embryological disorder with various degrees and directions of expression.
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PMID:Neurology of latent nystagmus. 142 90

Dissociated strabismus includes movements in the vertical, horizontal, and torsional axes. Dissociated vertical deviation (DVD) is an oversimplified label because it implies a purely vertical deviation. When the abducting component of the dissociated strabismus complex is prominent, the term dissociated horizontal deviation (DHD) is used. We present six patients with accommodative esotropia who developed prominent DHD. Only two patients have a prior history of congenital esotropia. Latent nystagmus was observed in five of the patients. With the combination of DHD and esotropia, an esodeviation during active fixation may become an exodeviation when the patient is visually inattentive. Five patients required surgery for DHD. Four options are used and discussed. DHD can be treated alone with lateral rectus muscle recession. DHD can be treated as above, but combined with medial rectus muscle recessions or posterior fixation sutures to simultaneously treat the esotropia. The esotropia can be treated alone, possibly with a reduced surgical dosage. If the patient varies from an esodeviation to an exodeviation, but is straight much of the day, observation without surgical therapy may be advisable. Just as a hypotropia can have an overlying DVD, an esotropia can have an overlying DHD. This combination may masquerade as variable angle esotropia or may present as an esodeviation when the patient is visually attentive and an exodeviation when the patient is visually inattentive.
J Pediatr Ophthalmol Strabismus
PMID:Dissociated horizontal deviation and accommodative esotropia: treatment options when an eso- and an exodeviation co-exist. 749 58

Infantile strabismus is accompanied by latent nystagmus, primary inferior oblique muscle overaction, and dissociated vertical divergence. If we examine the evolutionary underpinnings of these ocular rotations, we can construct a unifying mechanism for the sensorimotor abnormalities that arise in humans with infantile strabismus. Latent nystagmus, primary inferior oblique muscle overaction, and dissociated vertical divergence correspond to visual balancing reflexes that are operative in lateral-eyed animals in yaw, pitch, and roll, respectively. In humans with infantile strabismus, these subcortical visual reflexes are reactivated by a physiologic imbalance in binocular visual input, which resets central vestibular tone in 3-dimensional space. These visual reflexes reveal the evolutionary role of the eyes as sensory balance organs that can directly modulate central vestibular tone. Latent nystagmus, primary oblique muscle overaction, and dissociated vertical divergence should be reclassified as visuo-vestibular eye movements.
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PMID:Visuo-vestibular eye movements: infantile strabismus in 3 dimensions. 1595 86

Latent nystagmus (LN) and manifest latent nystagmus (MLN) are closely associated with early visual deprivation and strabismus. In both cases, the eyes oscillate horizontally in an involuntary manner and the fast phases always beat towards the attending or fixing eye. By simultaneously recording eye movements during the dichoptic viewing of dissimilar visual stimuli we present evidence that MLN offers a unique opportunity to examine the nature of sensori-motor switching. In particular, we show how the nystagmus beat direction is strongly influenced by endogenous and exogenous attention. A model describing the possible mechanisms underpinning the sensori-motor switching is proposed.
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PMID:Manifest latent nystagmus: a case of sensori-motor switching. 1871 45

Latent nystagmus (LN) is the by-product of fusion maldevelopment in infancy. Because fusion maldevelopment--in the form of strabismus and amblyopia--is common, LN is a prevalent form of pathologic nystagmus encountered in clinical practice. It originates as an afferent visual pathway disorder. To unravel the mechanism for LN, we studied patients and nonhuman primates with maldeveloped fusion. These experiments have revealed that loss of binocular connections within striate cortex (area V1) in the first months of life is the necessary and sufficient cause of LN. The severity of LN increases systematically with longer durations of binocular decorrelation and greater losses of V1 connections. Decorrelation durations that exceed the equivalent of 2-3 months in human development result in an LN prevalence of 100%. No manipulation of brain stem motor pathways is required. The binocular maldevelopment originating in area V1 is passed on to downstream extrastriate regions of cerebral cortex that drive conjugate gaze, notably MSTd. Conjugate gaze is stable when MSTd neurons of the right and left cerebral hemispheres have balanced binocular activity. Fusion maldevelopment in infancy causes unbalanced monocular activity. If input from one eye dominates and the other is suppressed, MSTd in one hemisphere becomes more active. Acting through downstream projections to the ipsilateral nucleus of the optic tract, the eyes are driven conjugately to that side. The unbalanced MSTd drive is evident as the nasalward gaze-holding bias of LN when viewing with either eye.
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PMID:The neural mechanism for Latent (fusion maldevelopment) nystagmus. 2081 6