Cases reported "Strabismus"

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21/46. Acquired esotropia as initial manifestation of arnold-chiari malformation.

    A 13-year-old patient originally presented with a divergence palsy and gaze-evoked nystagmus. Over a short period of time, the esotropia became increasingly comitant and was successfully treated with strabismus surgery. Three years later, she developed downbeat nystagmus. An arnold-chiari malformation could only be demonstrated using nuclear magnetic resonance imaging (MRI). Subsequent neurosurgical decompression resulted in resolution of the downbeat nystagmus with maintenance of single binocularity.
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22/46. The ETHAN syndrome.

    Two mechanisms by which patients compensate for congenital nystagmus are assumption of a head position that places the eyes in a "null zone" of least nystagmus, known as nystagmus compensation syndrome (NCS), and convergence to dampen nystagmus, known as nystagmus blockage syndrome (NBS). We followed five patients in two groups who combine these mechanisms. The first group presented with spontaneous alternation between nystagmus and a head turn with orthotropia (NCS), and a large-angle esotropia with a variable head position that persisted even when patched (NBS). The second group of patients presented with a constant large-angle esotropia that lessened their nystagmus and variable head posture (NBS). Following recession of both medial rectus muscles with or without placement of posterior fixation sutures, they developed an abnormal head posture with orthotropia (NCS). The presence of mild amblyopia may contribute to the alternation between the two compensatory mechanisms.
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23/46. Unilateral esotropia after enucleation in infancy.

    Five patients developed esotropia in the remaining eye after unilateral enucleation in the first few weeks to months of life. esotropia was associated with a face turn toward the opposite side and abduction nystagmus with a null point in extreme adduction. Our experience with these patients supports the reflexogenic theory for the development of a type of congenital-infantile esotropia. An intact globe-ocular muscle relationship, even in a blind eye, may have a stabilizing effect on the fellow eye in the first few weeks to months of life, and this should be considered before enucleation is done.
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24/46. Congenital nystagmus surgery. A quantitative evaluation of the effects.

    Nystagmus intensities at various gaze angles were studied both preoperatively and postoperatively, using accurate ocular motility recordings, in three cases of congenital nystagmus. In addition to shifting the nystagmus null, the surgery broadened the null region and resulted in an overall reduction in nystagmus intensity at all gaze angles. Surgical rotation also resulted in improved visual acuity in all cases. The postoperative acuity at 0 degrees was better than the preoperative acuity at both 0 degrees and the patient's preferred gaze angle (ie, the preoperative null angle). This was not only for the two patients who showed an improved preoperative acuity with their head turn but also for the patient whose preoperative acuity did not substantially improve with her preferred head turn. Eye movement recordings have made it possible to accurately determine the amount of surgery required and to predict acuity increases even when undetectable during the preoperative clinical examination.
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25/46. Voluntary vertical nystagmus.

    A patient with hypertropia caused by fourth-nerve palsy manifested primary position oscillations characteristic of voluntary nystagmus. This benign condition must be kept in mind even when dealing with primary position vertical nystagmus to avoid extensive and potentially dangerous investigations.
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26/46. Normalization of binocular VERs after early onset visual deprivation in man.

    Visually evoked responses (VERs) were elicited by a reversing checkerboard target from a patient who suffered early onset bilateral deprivation of form vision as a result of a high refractive error, large amplitude strabismus, and congenital nystagmus. Monocular and binocular steady-state VERs were abnormal in amplitude and wave form even when a correction for the patient's large refractive error (compound hyperopic astigmatism) was worn. Although monocular VERs could not be normalized, a normal wave form and amplitude were restored to the binocular VER by the addition of horizontal prisms to the patient's ophthalmic prescription. The initially degraded binocular VER gradually acquired a normal morphology and amplitude as the magnitude of compensating base-out prisms in the patient's habitual ophthalmic prescription was systematically increased. The relationship between the binocular VER amplitude and the correcting prisms derived by the method described in this paper was subsequently used to arrive at a practical clinical solution for the patient's unusual and debilitating visual symptoms. This electrophysiological evaluation of binocular function at the cortical level proved to be a very useful diagnostic procedure with prognostic value; standard clinic procedures were ineffective in elaborating the patient's sensory and oculomotor disorders. The theoretical and practical implications of managing patients with a history of early onset visual deprivation are discussed.
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27/46. Acquired esotropia. A manifestation of Chiari I malformation.

    A patient with acquired esotropia underwent apparently successful strabismus surgery. Subsequent recurrence of esotropia, associated with square-wave jerks and downbeat nystagmus led to further investigation. Although standard CT scan was normal, rescanning after instillation of metrizamide demonstrated a Chiari I malformation. Posterior fossa decompression alleviated the esotropia. Acquired esotropia has not been recognized as a manifestation of Chiari I malformation. Our case illustrates that a high degree of suspicion is required to make the diagnosis of Chiari I malformation. Specialized techniques, such as metrizamide cisternography, or magnetic resonance imaging may be necessary if routine diagnostic measures are unrevealing.
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28/46. Nystagmus blockage syndrome in the unilaterally blind patient.

    Those patients who have reduced vision in one eye and a variable esotropia should be suspected of having the nystagmus blockage syndrome. Typically such patients will have a head turn in the direction of the good eye with a preferred medial fixation point. Careful examination will reveal a nystagmus with the preferred position as the null point. Also, any patient who repeatedly has a recurrent esotropia after surgery should be suspected of having the nystagmus blockage syndrome. It is important to perform a posterior fixation suture with a recession on the medial recti of both eyes and to alter the null point by recessing the medial rectus more than 3 mm and resecting the lateral rectus appropriately for the head turn at the same surgical procedure. The eye with poor vision also should have the lateral rectus resected.
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29/46. 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.
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30/46. Manifest latent nystagmus of late onset: a case report.

    A case of manifest latent nystagmus of late onset in a 13-year-old girl is reported. The nystagmus became manifest during the development of a hypertropia of the left eye. The spontaneous nystagmus was successfully treated by surgical correction of the hypertropia. The observations are discussed with regard to theories on the origin of latent nystagmus.
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