Cases reported "Nystagmus, Pathologic"

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1/7. Osteopetrorickets: case report.

    We report the case of a baby girl who presented with rickets at 3 months. At the age of 5 months she was readmitted because of nystagmus and a diagnosis of osteopetrosis was made on the basis of clinical and radiological findings. rickets is a paradoxical feature of osteopetrosis resulting from inability to maintain a normal calcium-phosphorus balance. In our patient the onset of rickets before other symptoms of osteopetrosis suggests a primary defect. Conclusion: It is possible that patients with osteopetrosis and rickets (osteopetrorickets) represent a different mutation like the osteopetrosis mouse, which is the only animal mutation with rickets.
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2/7. See-saw nystagmus and brainstem infarction: MRI findings.

    A patient with see-saw nystagmus had a lesion localized by magnetic resonance imaging (MRI) to the paramedian ventral midbrain with involvement of the right interstitial nucleus of Cajal. This the first MRI study of see-saw nystagmus associated with a presumed brainstem vascular event. Our findings support animal and human studies suggesting that dysfunction of the interstitial nucleus of Cajal or its connections is central in this disorder.
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3/7. The changing direction of nystagmus in acute Meniere's disease: pathophysiological implications.

    The direction(s) and pathophysiologic basis of nystagmus during an acute attack of Meniere's disease have been subject to much debate in the world literature. Clinical recordings from two patients whose nystagmus was captured near the very beginning of the acute vertiginous episode are presented. Previous clinical observations in Meniere's disease, experimental animal models concerned with initiation of peripheral nystagmus, and the phenomenon of recovery are discussed.
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4/7. Omnipause neurons in two cases of opsoclonus associated with oat cell carcinoma of the lung.

    Opsoclonus is an involuntary eye movement disorder in which there are chaotic, usually conjugate, multidimensional saccadic eye movements. In this paper 2 cases of opsoclonus are reported, as a paraneoplastic phenomenon in association with oat cell carcinoma of the lung. It has previously been hypothesized that opsoclonus results from dysfunction of a group of premotor neurons in the brainstem called omnipause neurons. We describe the location of these cells in man by homology with animal studies, and describe the light microscopic appearance of these neurons in the 2 cases of opsoclonus. Although these neurons appeared normal it is still possible that their function was disturbed as a result of metabolic or neurotransmitter abnormalities.
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5/7. Periodic alternating nystagmus associated with albinism.

    We examined a 73-year-old woman with the rare association of albinism and (presumably) congenital periodic alternating nystagmus. The mechanism of the nystagmus in this case is uncertain. Anomalous retinogeniculate pathways have been documented in albino animals. Periodic alternating nystagmus might occur in some patients with albinism if there are also anomalies in the pathways conveying visual information to the cerebellum and brainstem.
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6/7. Slow build-up of optokinetic nystagmus associated with downbeat nystagmus.

    Eye movement recordings in two patients with downbeat nystagmus demonstrated an unusual finding of severely impaired smooth pursuit and relatively unimpaired optokinetic nystagmus (OKN). OKN was characterized by a remarkable, slow build-up of slow-component velocity, similar to that found in afoveate animals. Optokinetic after-nystagmus (OKAN), or transient persistence of nystagmus after cessation of visual stimulation, typical of the optokinetic response of normal human subjects, was also preserved in these patients. These observations suggest that the normal contribution of smooth pursuit to the ocular motor response to rotation of the visual environment can be selectively removed by a lesion at the level of the craniocervical junction.
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7/7. Bechterew's phenomenon in humans. A new explanation.

    Bechterew's phenomenon, or reversal of post-unilateral labyrinthectomy spontaneous nystagmus following subsequent contralateral labyrinthectomy in experimental animals, has been known for 100 years. However, it is rarely observed in humans. This paper describes Bechterew's phenomenon in a patient following successful mitral valve replacement and aorto-coronary bypass. The observations are compatible with a recent study which postulates that intervestibular commissural pathways, forming closed loops for neural signals between the vestibular nuclei, may be the main site for vestibular compensation which is associated with the recovery of balanced resting activity in the bilateral vestibular nuclei (Galiana 'et al., 1983). Using simple analytic arguments, it is found that compensation of nystagmus following unilateral labyrinthectomy, the Bechterew's phenomenon and its compensation, and recovery nystagmus could all result from long-term neural changes at the level of commissural connections.
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