Cases reported "Papilledema"

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1/51. pseudotumor cerebri in children receiving recombinant human growth hormone.

    PURPOSE: This article represents the first report in the ophthalmology literature of an association between pseudotumor cerebri (PTC) and recombinant human growth hormone (rhGH). DESIGN: Noncomparative case series. PARTICIPANTS: Three children receiving rhGH for short stature with turner syndrome, Jeune syndrome, or down syndrome. methods: Children underwent full ocular examination. After papilledema was identified, patients underwent lumbar puncture and imaging with either magnetic resonance imaging or computerized tomography. Treatment was under the guidance of the primary physician or neurosurgeon. The rhGH was discontinued in all children. MAIN OUTCOME MEASURES: visual acuity and evaluation of the optic nerve for resolution of papilledema were followed at each examination. RESULTS: In all three cases, papilledema resolved with the cessation of rhGH, and treatment with acetazolamide or prednisone. visual acuity was unchanged in case 1, decreased by two to three lines in case 2, and was inconsistent in case 3. One child (case 2) required a ventriculoperitoneal shunt for persistent elevation of intracranial pressure. CONCLUSION: There appears to be a causal relationship between the initiation of rhGH with the development of PTC. Children should have a complete ophthalmic evaluation if they report headache or visual disturbances. Baseline examination with routine follow-up should be instituted when children cannot adequately communicate.
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2/51. optic nerve edema as a consequence of respiratory disease.

    The authors describe a patient with bilateral papilledema, visual field abnormalities, poorly reactive pupils, meningeal enhancement on cranial MRI, and diffuse brain parenchymal hypervascularity. The opening pressure at the time of lumbar puncture was normal, and results of other CSF studies were normal. All abnormalities resolved with home oxygen therapy.
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3/51. papilledema and obstructive sleep apnea syndrome.

    OBJECTIVES: To characterize the pathogenesis and clinical features of optic disc edema associated with obstructive sleep apnea syndrome (SAS). methods: A series of 4 patients with SAS and papilledema (PE) underwent complete neuro-ophthalmologic evaluation and lumbar puncture. In 1 patient, continuous 24-hour intracranial pressure (ICP) monitoring was also performed. RESULTS: All 4 patients had bilateral PE that was asymmetric in 2. Three patients had optic nerve dysfunction, asymmetric in 1, unilateral in 2. Daytime cerebrospinal fluid pressure measurements were within normal range. Nocturnal monitoring performed in one patient, however, demonstrated repeated episodes of marked ICP elevation associated with apnea and arterial oxygen desaturation. CONCLUSIONS: We propose that PE in SAS is due to episodic nocturnal hypoxemia and hypercarbia resulting in increased ICP secondary to cerebral vasodilation. In these individuals, intermittent ICP elevation is sufficient to cause persistent disc edema. These patients may be at increased risk for developing visual loss secondary to PE compared with patients with obesity-related pseudotumor cerebri because of associated hypoxemia. The diagnosis of SAS PE may not be appreciated because daytime cerebrospinal fluid pressure measurements are normal and because patients tend to present with visual loss rather than with symptoms of increased ICP.
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4/51. When does low mean high? Isolated cerebral ventricular increased intracranial pressure in a patient with a Chiari I malformation.

    OBJECTIVE: To present an unusual case of pseudotumor cerebri with increased intracranial pressure isolated to the cerebral ventricles resulting from a Chiari I malformation. MATERIALS AND methods: The patient received a complete ophthalmologic examination on initial presentation and subsequent visits, including visual acuity, pupillary examination, intraocular pressures, dilated fundus examination with assessment of degree of papilledema, and visual field testing. intracranial pressure was measured by lumbar puncture and subsequently by intracranial pressure bolt monitoring. magnetic resonance imaging (MRI) was used to diagnose the Chiari I malformation. RESULTS: The patient initially presented with bitemporal headaches, elevated opening pressure on lumbar puncture, and mild papilledema with a normal MRI. After lumboperitoneal shunt placement and several revisions, the patient presented with decreased vision OD secondary to Terson syndrome and worsening papilledema. Subsequent evaluation revealed normal lumbar opening pressures and a Chiari I malformation. She underwent ventriculoperitoneal shunt placement with resolution of her symptoms. CONCLUSIONS: Tonsillar herniation is a well-documented complication of lumboperitoneal shunt revision. Obstruction of cerebrospinal flow through the foramina of Magendie and Luschka can result in increased intracranial pressure isolated to the cerebral ventricles. In a patient with signs and symptoms of increased intracranial pressure but normal lumbar opening pressure, a Chiari I malformation should be suspected, particularly with a history of multiple lumboperitoneal shunt revisions.
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5/51. Asymptomatic idiopathic intracranial hypertension in young children.

    Presenting symptoms of idiopathic intracranial hypertension are known to vary with age. Older children may complain of headache, neck pain, diplopia, intracranial noises, or transient visual obscurations. Younger children may present with apathy or irritability. This report describes three young children with no obvious relevant symptoms in whom papilledema was newly found on routine follow-up eye examination for unrelated problems. At presentation, all had early papilledema with negative cranial neuroimaging studies. All remained apparently asymptomatic, but the papilledema progressed. Sedated lumbar puncture showed elevated cerebrospinal fluid pressure in all three. Two were felt to have truly idiopathic intracranial hypertension, whereas the third had jugular venous obstruction. The papilledema responded to treatment with either acetazolamide or furosemide in all three. An apparent lack of symptoms does not rule out chronic increased intracranial pressure in young children.
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6/51. Bilateral optic disk edema and blindness as initial presentation of acute lymphocytic leukemia.

    PURPOSE: To report bilateral optic disk edema and blindness as the unusual initial presentation of acute lymphocytic leukemia (ALL) in an adult. methods: A 19-year-old man presented with a history of headaches, back pain, and 10 days of worsening vision that progressed to blindness. Ocular examination revealed light perception acuity in the right eye and no light perception in the left eye. Fundus examination revealed bilateral profound optic disk edema, tortuous vessels, and retinal hemorrhages. Acute lymphocytic leukemia was diagnosed with complete blood count and bone marrow biopsy. Head computed tomography and magnetic resonance imaging, were normal. Lumbar puncture revealed normal opening pressure. Ocular ultrasonography showed bilateral optic nerve enlargement. DESIGN: Interventional case report and literature review. ESULTS: The presumptive diagnosis of leukemic infiltration of the optic nerves was made, and urgent radiotherapy, intrathecal methotrexate, and intravenous daunorubicin were instituted. visual acuity improved to hand motions in the right eye. CONCLUSIONS: Acute lymphocytic leukemia can rarely present in adults as visual changes due to leukemic optic nerve infiltration. radiation treatment should be considered as an urgent treatment modality for this rare condition.
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7/51. Acquired hyperopia with choroidal folds.

    Acquired hyperopia with choroidal folds is an uncommon but well recognized condition that is often benign and classically shows flattening of the posterior pole of the affected eye, variable enlargement of the optic nerve complex, and a space between the optic nerve and its sheath. A case is presented that shows the perineural space is best seen on magnetic resonance imaging. Lumbar puncture to exclude increased intracranial pressure should be performed even in the absence of papilloedema.
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8/51. Severe papilledema identified 3 weeks after head injury.

    A 62-year-old woman presented with rapidly developed visual disturbance without associated headache or nausea 3 weeks after head injury. Ophthalmologic examination revealed bilateral severe papilledema with retinal hemorrhage, and intracranial pressure (ICP) was 17.5 cmH2O estimated by lumbar puncture. Computed tomography and magnetic resonance (MR) imaging showed no evidence of increased ICP, except dilation of the subarachnoid space around the optic nerves with distortion of the nerves. Her visual acuity remarkably improved after steroid and glycerol treatment, and optic fundus examination revealed bilateral clear optic papillae without atrophic changes. Follow-up MR imaging demonstrated that the bilateral optic nerves had regained the normal appearance. These results indicate that the bilateral papilledema was caused by increased subarachnoid pressure around the bilateral optic nerves. We conclude that papilledema can occur with a mildly increased ICP and trapped subarachnoid cerebrospinal fluid around the optic nerves, and papilledema may progress after the ICP is normalized. papilledema is a warning sign for increased ICP, associated with future visual loss from retinal hemorrhage. Therefore, repeated funduscopic investigation is necessary for the early diagnosis and treatment of papilledema.
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9/51. pseudotumor cerebri in a patient with Goldenhar's and Duane's syndromes.

    A 4-year-old boy presented with Goldenhar's syndrome, Duane's syndrome and bilateral papilledema. magnetic resonance imaging of the brain was unremarkable. On lumbar puncture, the cerebrospinal fluid (CSF) pressure measured 36 cm H(2)O. CSF examination was normal. The diagnosis of pseudotumor cerebri was made, and treatment with acetazolamide was started. As the papilledema did not resolve, steroids were added to the treatment. Lumbar puncture was repeated after 1 month, and pressure was found to be 30 cm H(2)O. Because medical treatment was not effective in lowering the CSF pressure, optic nerve sheath fenestration was performed. papilledema resolved over the next 2 months. To the best of our knowledge, this is the first case of Goldenhar's syndrome associated with pseudotumor cerebri.
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10/51. papilledema as the presenting manifestation of spinal schwannoma.

    A 63-year-old woman with headache, blurred vision, bilateral optic disc edema, and normal cranial magnetic resonance imaging scan underwent lumbar puncture that revealed an elevated opening pressure (290 mm water), a protein level of 114 mg/dl, and mild pleocytosis. Spinal magnetic resonance imaging later demonstrated a sacral tumor, which proved to be a schwannoma with sarcoid-like features. After surgical removal of the tumor, the patient's manifestations resolved. This case emphasizes that low spinal cord tumors can cause elevated intracranial pressure without causing markedly elevated cerebrospinal fluid protein or cells, or any myelopathic manifestations, perhaps by obstructing sacral cerebrospinal drainage. Comprehensive spine imaging should be a part of the evaluation of a patient with papilledema who has normal brain imaging but abnormal spinal fluid constituents.
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