Cases reported "Ocular Motility Disorders"

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1/84. Fresnel membrane prisms: clinical experience.

    BACKGROUND: There are few published reports on the clinical application of Fresnel membrane prisms in the treatment of diplopia in adults. The authors describe the use of these prisms in patients with fourth and sixth cranial nerve palsies, restrictive motility caused by thyroid-related orbital disease, and convergence insufficiency. methods: Of 209 patients who had been treated with Fresnel prisms, 141 were selected. The database included patients from a private practice in Montreal, seen from 1988 to 1996, and patients seen by orthoptists in the ophthalmology department of a children's hospital in Montreal between 1992 and 1996. All the patients had diplopia associated with fourth (48 patients) or sixth (43 patients) cranial nerve palsy, thyroid-related orbitopathy (18 patients) or convergence insufficiency (32 patients). After qualitative and quantitative assessment of the ocular misalignment, a Fresnel prism was selected for power and axis and for appropriate location on the spectacle lens. Ocular dominance and side of paresis or restriction were also considered in the placement of the prism. The patient's response to treatment was documented. RESULTS: The Fresnel prisms were oriented horizontally in 72 patients (51%), vertically in 55 (39%) and obliquely in 14 (10%). They were placed on the spectacle lens before the nondominant eye in 127 cases (90%), either covering the entire lens, or on the upper or lower segment or both. The patients were followed for an average of 15 (range 2 to 96) months. Of the 141 patients 113 (80%) had a successful outcome, with relief of their diplopia. Twenty-seven patients (19%) eventually had the prismatic correction ground into the lens, 70 (50%) chose to wear the Fresnel prism on a permanent basis because incorporation into the lens was not possible or because of cost, and 17 (12%) used the Fresnel prism as a temporary device before or after surgery. Most patients who converted to incorporated prisms did so when the prismatic power became stable, usually after 6 to 8 months. Eight patients (6%) stopped using the prism because of associated side effects, such as blurred vision, persistent diplopia, torsion or optical aberrations. INTERPRETATION: The Fresnel prism is an excellent device in treating diplopia in adult patients. It is a reasonable permanent option when incorporating the prism into the spectacle lens is not possible. A fused blurred image caused by a Fresnel prism placed in front of the nondominant eye is preferable to double but clear images.
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ranking = 1
keywords = palsy
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2/84. Benign aqueductal cyst causing bilateral internuclear ophthalmoplegia after external ventricular drainage. Case report.

    The introduction of magnetic resonance (MR) imaging to the field of neuroimaging has allowed detection of various lesions that cause aqueductal stenosis. The authors report the case of a 3-year-old boy in whom a benign ventricular cyst developed in the aqueduct. The patient became drowsy after having complained of headache and vomiting; MR imaging revealed mild triventricular dilation and a normal-sized fourth ventricle. Repeated MR imaging performed 1 week later revealed an aqueductal cyst that had markedly enlarged during the intervening period. An external ventricular drainage system was installed, but recovery of consciousness in the child was unsatisfactory and a new bilateral internuclear ophthalmoplegia developed. Fenestration of the cyst wall and placement of a ventriculocisternostomy in the third ventricle were performed simultaneously by using a flexible neuroendoscope. By 2 weeks postsurgery, the patient's neurological symptoms had completely resolved. This case illustrates that simple rerouting of ventricular cerebrospinal fluid (CSF) can aggravate the symptoms of this rare lesion by causing severe compression of periaqueductal structures by a cyst that maintains a high intracystic pressure. Endoscopic surgery was an excellent choice of treatment to achieve both cyst fenestration and normalization of intracranial CSF pressure by creating a ventriculocisternostomy.
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ranking = 944.64301107157
keywords = ophthalmoplegia
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3/84. Unilateral thalamic infarction and vertical gaze palsy: cause or coincidence?

    Although vertical gaze palsy (VGP) is commonly associated with lesions of the rostral mesencephalon, there is some evidence that VGP may also be caused by a unilateral thalamic lesion. The case of a 68-year-old man with persistent upward gaze palsy after a unilateral thalamic infarction, demonstrated on computed tomography and magnetic resonance imaging scans, is presented. Subsequent high-resolution magnetic resonance scanning, however, showed involvement of the rostral mesencephalon as well. The authors suggest that in previous patients with VGP ascribed to a unilateral thalamic infarction, a coexisting mesencephalic involvement may have been missed because of inappropriate imaging techniques. Strong evidence of unilateral thalamic infarction as a cause of VGP is still lacking.
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ranking = 6
keywords = palsy
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4/84. Clinicopathological study of atypical motor neuron disease with vertical gaze palsy and ballism.

    The case of a 38-year-old patient with rapidly progressing motor neuron disease, complicated by major dysfunction of the extrapyramidal system and of vertical gaze is described. Neuropathological examination revealed a degenerative process that severely affected the lower motor neurons, as well as the neurons of the pars compacta of the substantia nigra, the nucleus of Darkschewitsch, the nucleus interstitialis of Cajal, the colliculi superiores, and the pallidum. The long tracts were unaffected at all levels of the brain stem and spinal cord. There was no convincing evidence for the presence of a multiple system atrophy or progressive supranuclear palsy; the results rather revealed a pattern of vulnerability characteristic of a variant of motor neuron disease.
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ranking = 643.34963623021
keywords = supranuclear, progressive supranuclear, supranuclear palsy, palsy
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5/84. Case report: one-and-a-half-syndrome and tuberculosis of the pons in a patient with AIDS.

    A patient with advanced AIDS presented with right conjugate gaze palsy and impaired adduction on left gaze (the one-and-a-half syndrome). The responsible pontine lesion involved the ipsilateral abducens nucleus and the adjacent medial longitudinal fasiculus (MLF), as demonstrated by magnetic resonance imaging (MRI). tuberculosis (TB) was the etiology of the brainstem lesion. The patient had complete recovery after anti-tuberculosis treatment. The nuclear location of the tuberculoma is unusual and the reversal of this neuro-ophthalmologic syndrome is noteworthy.
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ranking = 1
keywords = palsy
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6/84. Eye deviation in patients with one-and-a-half syndrome.

    To understand malalignments of the visual axes in one-and-a-half syndrome, we measured eye positions in 4 patients with this syndrome under two conditions: with Frenzel goggles to prevent eye fixation and without Frenzel goggles. When fixation was prevented with the Frenzel goggles, all patients showed mild outward deviation in both eyes. Removal of the Frenzel goggles elicited adduction of the eye ipsilateral to the side of the lesion for fixation, with greater outward deviation of the contralateral eye (acute stage), or adduction of both eyes to midposition for biocular fixation (convalescent stage). In 3 patients whose outward eye deviation with Frenzel goggles was greater on the ipsilateral side, a transition from one-and-a-half syndrome to ipsilateral internuclear ophthalmoplegia was noted, whereas a transition to ipsilateral gaze palsy was seen in the one patient whose deviation was greater on the contralateral side. These findings suggest that in one-and-a-half syndrome patients, the eyes tend to be in divergent positions when fixation is prevented; ipsilateral eye deviation may result from medial longitudinal fasciculus involvement, and contralateral eye deviation may result from paramedian pontine reticular formation involvement. Viewing a target may lead to a secondary deviation or adaptation of eye positions for fixation.
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ranking = 189.92860221431
keywords = ophthalmoplegia, palsy
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7/84. Total recovery after bilateral paramedian thalamic infarct.

    Bilateral paramedian thalamic infarcts are characterised initially by the association of acute vigilance disorders and vertical gaze palsy, followed by persisting dementia with severe mnemic disturbance, global aspontaneity and apathy. We describe a patient with a dramatic neuropsychological recovery, confirmed by testing examination and completed by a cerebral metabolism study. The pathophysiology of this type of cognitive deficit is discussed.
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ranking = 1
keywords = palsy
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8/84. July 2000: A 70 year old with rigidity, decreased ocular movements, and dementia.

    The July Case of the Month (COM): A 70 year old male presented with a four year history of cognitive decline, difficulty expressing himself, and an increasingly unsteady gait with numerous falls. At presentation he was wheel-chair bound. Examination showed some slowing of speech, mild memory impairment, but normal cranial nerves. Spastic weakness and brisk reflexes were also noted, with bilateral ankle clonus. MRI scans were normal. Four years later he was admitted with a urinary tract infection and was mute with severely impaired ocular motility. He died 18 months later and autopsy showed the classic neuropathological findings of typical Progressive supranuclear palsy, including tau-positive glial inclusions.
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ranking = 453.41309647037
keywords = supranuclear, supranuclear palsy, palsy
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9/84. Complete bilateral horizontal gaze paralysis disclosing multiple sclerosis.

    Two women presented with bilateral internuclear ophthalmoplegia evolving in a few days to complete bilateral horizontal gaze paralysis. Convergence and vertical eye movements were normal. Cerebral MRI showed a few small white matter lesions in the lateral ventricle regions, and, at the brainstem level, a single, small, bilateral lesion affecting the posterior part of the medial pontine tegmentum and responsible for the clinical syndrome. The condition gradually improved in both patients, following a similar progression as at the onset: improvement first involved the adduction movements in both eyes, whereas bilateral abduction paresis still persisted for a few weeks, before complete recovery of eye movements. Bilateral damage to the medial longitudinal fasciculus and subsequent lateral extent of damage to the region of the two abducens emerging fibres may explain the clinical findings. In both cases, the cause was probably multiple sclerosis.
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ranking = 188.92860221431
keywords = ophthalmoplegia
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10/84. Visual impairment due to a dyskinetic eye movement disorder in children with dyskinetic cerebral palsy.

    Neurological lesions that cause dyskinetic cerebral palsy (CP) commonly involve ocular movements. This report describes a group of 14 children (nine males, five females) whose CP is associated with severe dyskinetic eye movements. Ages ranged from 4 months to 13 years (mean 6.9 years). Clinical features of this eye movement disorder are discussed and defined. The visual function of these children is slow, variable, and highly inefficient. They are often misdiagnosed as blind, due to cortical visual impairment. Early recognition of dyskinetic eye moment disorder and appropriate developmental and educational management are important.
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ranking = 5
keywords = palsy
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