Cases reported "Ophthalmoplegia"

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1/11. Pupillary areactivity in hydrocephalus of recent onset.

    A patient who presented with bilateral loss of all pupillary reactions and normal ocular motor function is reported. Investigation revealed the presence of massive hydrocephalus. The syndrome developed shortly after transsphenoidal surgery for a suprasellar craniopharyngioma. Pupillary function returned to normal following the insertion of a ventriculo-peritoneal shunt. It is suggested that the syndrome was due to compression of the visceral oculomotor nuclei by a dilated sylvian aqueduct.
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2/11. Bilateral traumatic third nerve palsy.

    Bilateral palsy of the third cranial nerve in a head-injured patient is described. Delayed computed tomography scanning demonstrated a midline necrotic lesion within the mesencephalon ventral to the aqueduct. The lesion, possibly the sequela of a focal contusion, involved both third nerve nuclear complexes and caused paralysis of their voluntary as well as autonomic functions. Gaze mechanisms and long tracts appeared to be less heavily damaged. The literature dealing with third nerve palsy, particularly bilateral cases, from traumatic and other origins is briefly reviewed.
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3/11. Reversibility of Parinaud syndrome in thalamic hemorrhage.

    Parinaud syndrome, associated with a left thalamic hemorrhage, disappeared completely in a 57-year-old woman after ventriculoperitoneal shunt. The syndrome may be attributed to increased intracranial pressure owing to mass effect on the pretectal region and tectum, or to tightness in the incisura causing hydrocephalus secondary to aqueduct compression. The lesions responsible for the syndrome may not be irreversible.
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4/11. Upgaze paralysis caused by lesion of the periaqueductal gray matter.

    A 61-year-old man with upgaze paralysis was found on postmortem examination to have had a single lesion of the brain stem confined to the periaqueductal gray matter between the levels of the superior and inferior colliculi. Most previous neuropathologic cases reported in human beings have consisted of much larger lesions with common involvement of the posterior commissure and pretectum. We suggest that the lesion in this case caused upgaze paralysis either by interrupting descending fibers from the interstitial nucleus of Cajal or by destroying neurons located within the periaqueductal gray matter.
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keywords = aqueduct
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5/11. The Sylvian aqueduct syndrome and neurofibromatosis.

    A 23-year-old man initially presented with the Sylvian aqueduct syndrome and subsequently developed cutaneous neurofibromata. The case is reported and the possibility that these represent manifestations of the same genetic abnormality is discussed.
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6/11. Parinaud's syndrome in hydrocephalus due to a basilar artery aneurysm.

    A 65-year-old woman appeared with a progressive dementia, gait disturbance, and Parinaud's syndrome. A computed tomography scan, an angiogram of the vertebral artery, and metrizamide ventriculography demonstrated a marked hydrocephalus. A giant aneurysm at the termination of the basilar artery projected into the third ventricle producing partial obstruction of the aqueduct. The symptoms were resolved by a ventriculoperitoneal shunt; but after a month, the patient again showed the upward-gaze palsies concomitant with occurrence of shunt malfunction. The possible mechanisms of Parinaud's syndrome observed in the patient are discussed.
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keywords = aqueduct
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7/11. Neuro-ophthalmological complications of enlargement of the third ventricle.

    A wide variety of visual sensory and ocular motor problems may occur as a direct result of enlargement of the third ventricle. Four patients are described with optic nerve dysfunction, partial third nerve palsy, proptosis, and Sylvian aqueduct syndrome all resulting from an enlarged third ventricle. The pathogenetic mechanisms are discussed.
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8/11. The supranuclear disturbances of gaze in kernicterus.

    Five patients with kernicterus and ocular motility disturbances are reported. All of the patients showed some defect in vertical gaze but not always upgaze. The most severely affected patient exhibited slowness of horizontal saccades in addition to a total vertical gaze palsy. In general, the severity of the ocular motility disturbance paralleled the severity of hearing loss. It is suggested that damage to the periaqueductal area accounts for disturbances in vertical gaze and the infrequent horizontal saccadic disturbances results from interruption of the descending centrifugal fibers. It is emphasized that kernicterus must be included in the differential diagnosis of any supranuclear vertical gaze disturbance.
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keywords = aqueduct
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9/11. Down gaze palsy due to periaqueductal lesion diagnosed by magnetic resonance imaging.

    Selective paralysis of downward gaze is known to be rare. There are 6 cases reported in the literature based on neuropathologic and anatomical studies. We report a 60-year-old diabetic and hypertensive patient with isolated down gaze palsy. Computed tomography failed to show the lesion in the periaqueductal region, and the diagnosis was made by magnetic resonance imaging. The case presented is the only one still surviving.
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keywords = aqueduct
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10/11. Mesencephalic clefts with associated eye movement disorders.

    OBJECTIVE: To describe two patients with mesencephalic midline clefts and associated eye movement disorders. DESIGN: case reports. RESULTS: The first patient developed bilateral internuclear ophthalmoplegia with exotropia, reduced convergence, right ptosis, right fourth-nerve palsy, and right elevator palsy several years after meningitis with hydrocephalus. The second patient had bilateral internuclear ophthalmoplegia with exotropia, reduced convergence, bilateral ptosis, limited upward gaze, and right hypertropia since childhood. In both patients, magnetic resonance imaging showed a midline cleft extending from the cerebral aqueduct into the midbrain. CONCLUSION: It is likely that the clefts affected the oculomotor nuclei and medial longitudinal fasciculi, accounting for the eye movement disorders.
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