Cases reported "Diplopia"

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1/14. Pathologic causes of the superior oblique click syndrome.

    PURPOSE: To describe the clinical features in two patients with superior oblique click syndrome and the pathologic causes of their symptoms. DESIGN: Two observational case reports. PARTICIPANTS: Two patients. methods: The clinical histories, results of physical examinations, treatment, and pathologic findings in two patients with superior oblique click syndrome are reviewed and analyzed with reference to the literature. MAIN OUTCOME MEASURES: Relief of symptoms. RESULTS: Both patients were operated on; one was found to have a schwannoma and the other a giant cell tumor of tendon sheath as causes of their symptoms. Symptoms were relieved by removal of the lesions and have not recurred. CONCLUSION: Definite pathologic lesions may cause the superior oblique click syndrome.
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2/14. Malignant pilocytic astrocytoma in the medulla oblongata: case report.

    A 27-year-old woman visited our hospital with chief complaints of abducens nerve palsy and cerebellar symptoms. On computerized tomographic scanning and magnetic resonance imaging, a tumor with strong enhancement was found on the dorsal side of the medulla oblongata. A tumor was excised by suboccipital craniotomy and C1 laminectomy. Histologically, many Rosenthal fibers together with pilocytic tumor cells were found in some regions, but a very high Ki-67 labeling rate accompanied by cells with nuclei of irregular size and giant cells was observed in other regions. The tumor was diagnosed as malignant pilocytic astrocytoma originating from pilocytic astrocytoma by transformation. The biological behavior of pilocytic astrocytoma is obscure in several respects. We report our experience of a case of malignant pilocytic astrocytoma that developed in the brain stem and progressed extremely rapidly.
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keywords = giant
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3/14. erdheim-chester disease: two cases of orbital involvement.

    erdheim-chester disease (ECD) is an increasingly recognised form of fibro-inflammatory process characterised by xanthomatous histiocytes containing large amounts of ingested lipid, plasma cells, macrophages and Touton-type giant cells. Ophthalmic involvement in ECD has been reported in only 22 cases. We describe two patients, one presenting with diabetes insipidus and subsequently developing orbital pseudotumours and retroperitoneal fibrosis, the other presenting with exophthalmos and diplopia. The first patient was treated with cladribine and subsequently developed sudden onset of bilateral blindness while the second required radiation therapy for the retro-orbital process and developed radiation retinopathy. These cases typify the variable presentation and course in patients with ECD.
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4/14. Choroidal infarction, anterior ischemic optic neuropathy, and central retinal artery occlusion from polyarteritis nodosa.

    PURPOSE: Ocular ischemia from polyarteritis nodosa (PAN) is rare. The authors present a case of multifocal ocular infarction from PAN. methods AND RESULTS: A 70-year-old woman developed hand and foot numbness followed by intermittent blurred vision and binocular horizontal diplopia. Two weeks later, she suddenly lost vision in the right eye from a central retinal artery occlusion and then developed a left anterior ischemic optic neuropathy and bilateral triangular choroidal abnormalities consistent with infarction. Her erythrocyte sedimentation rate and c-reactive protein were elevated. Although giant cell arteritis was suspected, a multiple mononeuropathy was demonstrated by electromyogram and nerve conduction velocity studies. biopsy specimens from her sural nerve and biceps muscle showed a necrotizing vasculitis with fibrinoid necrosis, consistent with PAN. CONCLUSIONS: polyarteritis nodosa can produce ischemia of a variety of ocular structures, including the retina, choroid, and optic nerve. In our patient, all three structures were affected. To our knowledge, this is the first reported case of the triangular sign of Amalric in PAN.
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5/14. Herpes zoster vasculitis presenting as giant cell arteritis with bilateral internuclear ophthalmoplegia.

    PURPOSE: To present a case of herpes zoster vasculitis presenting as giant cell arteritis. DESIGN: Interventional case report. methods: A 77-year-old woman presented with sudden onset of diplopia associated with temple headaches and a previous history of herpes zoster ophthalmicus. A temporal artery biopsy was obtained and in-situ hybridization performed for herpes zoster dna. RESULTS: The patient presented with a bilateral internuclear ophthalmoplegia. Initial diagnostic evaluation, including erythrocyte sedimentation rate, c-reactive protein, and temporal artery biopsy, was consistent with giant cell arteritis. However, in-situ hybridization of the temporal artery specimen was positive for herpes zoster dna. CONCLUSIONS: Herpes zoster vasculitis may mimic giant cell arteritis and should be considered in the differential of any patient with presumed giant cell arteritis with suspicious findings, central nervous system involvement, or previous herpes zoster infection.
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6/14. A case of giant expanding cephalhematoma: does the administration of blood coagulation factor XIII reverse symptoms?

    BACKGROUND: The mechanism of continuous massive hemorrhage into the subperiosteal space in children without coagulation defects is unknown. We report a case of giant expanding cephalhematoma reversed by the administration of blood coagulation factor XIII concentrate. METHOD: The patient was an 8-year-old boy with a history of minor head trauma who developed a giant expanding cephalhematoma with intraorbital extension. The laboratory data showed severe anemia, but a routine blood coagulation test showed no abnormalities except for a low factor XIII level. RESULT: The administration of factor XIII concentrate completely reversed the symptoms in 2 weeks. CONCLUSION: We speculate that one of the possible mechanisms of cephalhematoma expansion without blood coagulation defects might be acquired factor xiii deficiency from severe hemorrhage in a hematoma.
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ranking = 6
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7/14. Thrombosed giant intracavernous aneurysm with subsequent spontaneous ipsilateral carotid artery occlusion.

    We report a case of a 47-year-old man with a giant thrombosed aneurysm of the right cavernous internal carotid artery who initially presented with headache, double vision and trigeminal numbness. He experienced subsequent asymtomatic proximal occlusion of the parent vessel, revealed by follow-up angiography. This case illustrates the possibility that a giant thrombosed aneurysm may exert enough compression upon the parent vessel to induce flow stasis with resultant intraluminal thrombosis progressing to occlude the entire parent artery.
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8/14. Intracavernous carotid aneurysm--an unusual cause of isolated abducens nerve palsy.

    We discuss the case of a 59-year-old woman who presented to the emergency department with complaints of diplopia for five days. physical examination disclosed an isolated complete right abducens nerve palsy. angiography revealed a giant aneurysm from the postcavernous portion of the right internal carotid artery. This case illustrates an unusual etiology of a unilateral abducens nerve palsy.
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9/14. Internuclear ophthalmoplegia in giant cell arteritis.

    ophthalmoplegia from ischemia to peripheral ocular motor nerves or muscles may complicate the course of giant cell arteritis (GCA). Although brainstem ischemia is known to occur in GCA, internuclear ophthalmoplegia has not been described. Two cases of biopsy-proven GCA are described in which internuclear ophthalmoplegia resulted from brainstem ischemia. Embolization from thrombosed extradural segments of inflammed vertebral arteries, or arteritis of brainstem perforating vessels may account for brainstem infarction. Rapid tapering of steroids was temporally related to brainstem infarction in both cases.
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keywords = giant
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10/14. Bilateral internuclear ophthalmoplegia--an unusual initial presenting sign of giant cell arteritis.

    A 63-year-old man presented six days after the sudden onset of horizontal double vision. His left eye became divergent two days later. On initial examination he had bilateral internuclear ophthalmoplegia with weakness of adduction and abducting nystagmus. Convergence was weak but there were no other neuro-ophthalmic signs. Constitutional signs included confusion and unsteadiness on his feet. A provisional diagnosis of arteritis was made. His ESR was 92 mm/h and a superficial temporal artery biopsy confirmed the diagnosis of giant cell arteritis. After two weeks or oral prednisolone his eye movements returned to normal. There have been no further relapses. This would appear to be a unique presentation of giant cell arteritis. The causes of internuclear ophthalmoplegia are discussed along with a review of the ocular and neuro-ophthalmic signs of giant cell arteritis.
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