Cases reported "Blindness"

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1/95. blindness from bad bones.

    Progressive visual loss is the most common neurologic finding in osteopetrosis. Several mechanisms may explain this phenomenon, including compression of the optic nerves caused by bony overgrowth of the optic canals and retinal degeneration. We report a child with osteopetrosis and progressive visual loss, even though patent optic canals were demonstrated by computed tomography and digital holography. This patient's visual loss was caused by increased intracranial pressure secondary, to obstruction of cerebral venous outflow at the jugular foramen. This case points to the importance of a full evaluation of the skull base foramina in the diagnostic workup of visual loss in patients with osteopetrosis.
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2/95. Reversible neuropraxic visual loss induced by allergic aspergillus flavus sinomycosis.

    This work reports a patient with visual loss treated successfully with surgical removal of the aspergillus flavus sinomycosis. Vision was partially reversed within hours after surgery before starting planned corticosteroid therapy. The patient's visual acuity continued to improve steadily until it became equal to that of the other eye. The immediate gain in vision and continued improvement without corticosteroid therapy suggest a new hypothesis for visual loss induced by allergic sinonasal aspergillosis. Simple mechanical pressure alone of the aspergillus mass over the nerve can produce visual loss, and this loss is reversed by removing the mass without corticosteroid therapy.
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3/95. Visual loss in idiopathic intracranial hypertension after resolution of papilledema.

    PURPOSE: To demonstrate that progressive visual field loss may occur after resolution of papilledema in patients with idiopathic intracranial hypertension and persistently elevated intracranial pressure. methods: A patient with idiopathic intracranial hypertension was evaluated with serial Humphrey automated static perimetry after initial treatment and resolution of papilledema. RESULTS: The patient developed recurrent headache and elevated cerebrospinal fluid pressure. optic nerve head appearance did not change. Automated perimetry demonstrated reproducible, worsening visual field loss; mean deviation decreased 11 dB in each eye. Visual field defects resolved after optic nerve sheath fenestration. CONCLUSIONS: Increased intracranial pressure caused visual field loss after resolution of papilledema. optic nerve sheath fenestration improved visual function in this patient.
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4/95. Progressive visual loss and ophthalmoplegia.

    A 51-year-old woman with hyperthyroidism presented with a 4-week history of bilateral progressive visual loss despite treatment with oral prednisone. Her visual function improved after bilateral orbital decompression. The indications for and advantages and disadvantages of radiation therapy and orbital decompression in TAO are discussed. The management of intraocular pressure, strabismus, and lid abnormalities in TAO is also addressed.
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5/95. Bilateral angle closure glaucoma and visual loss precipitated by antidepressant and antianxiety agents in a patient with depression.

    A 71-year-old woman with depression had been treated with an antidepressant (maprotiline) and antianxiety agents (clotiazepam and alprazolam). She had previously complained of ocular pain and blurred vision. However, thorough ocular examination was not performed at those times. On examination, visual acuity was no light perception OD and hand motion OS. Intraocular pressures were 33 mm Hg OU. Moderately dilated pupils, atrophic irises, shallow anterior chambers and closed angles were seen in both eyes. Despite treatment, her visual acuity decreased to no light perception bilaterally. Psychiatrists and ophthalmologists should be aware that antidepressants and antianxiety agents can precipitate angle closure glaucoma in susceptible eyes.
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6/95. Optic neuropathy in children with lyme disease.

    Involvement of the optic nerve, either because of inflammation or increased intracranial pressure, is a rare manifestation of lyme disease. Of the 4 children reported here with optic nerve abnormalities, 2 had decreased vision months after disease onset attributable to optic neuritis, and 1 had headache and diplopia early in the infection because of increased intracranial pressure associated with Lyme meningitis. In these 3 children, optic nerve involvement responded well to intravenous ceftriaxone therapy. The fourth child had headache and visual loss attributable to increased intracranial pressure and perhaps also to optic neuritis. Despite treatment with ceftriaxone and steroids, he had persistent increased intracranial pressure leading to permanent bilateral blindness. Clinicians should be aware that neuro-ophthalmologic involvement of lyme disease may have significant consequences. If increased intracranial pressure persists despite antibiotic therapy, measures must be taken quickly to reduce the pressure.
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7/95. Visual outcome of malignant hypertension in young people.

    A retrospective review was carried out of patients under 16 years old with malignant hypertension, who had been referred to a teaching hospital ophthalmology department because of reduced visual acuity. Four patients (three girls, one boy) were seen between 1994 and 2000 with a mean age at presentation of 11.5 years (range 9-15). In the short term, visual acuity improved after control of blood pressure in all four patients. However, in the long term, two patients were registered blind one to two years after presentation, one because of a choroidal neovascular membrane developing at the macula, and the other because of progressive optic neuropathy. Both of these patients had a longer duration of symptoms before diagnosis, worse visual acuity, and higher blood pressure at presentation when compared with the patients who made a good visual recovery. These observations suggest that early diagnosis of malignant hypertension in children is essential in reducing the likelihood of permanent severe visual damage.
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8/95. Catastrophic antiphospholipid antibody syndrome manifesting as an orbital ischemic syndrome.

    Painful bilateral ophthalmoparesis, marked proptosis, increased intraocular pressure, and blindness developed in a 29-year-old woman with protein c deficiency and catastrophic antiphospholipid syndrome. magnetic resonance imaging of the orbits showed bilateral proptosis, globe tenting, and tethering of the optic nerves consistent with an orbital ischemic syndrome. Despite aggressive therapy for antiphospholipid syndrome, the patient died. The autopsy showed necrosis of orbital tissues. This is the first report of orbital ischemic syndrome from protein c deficiency and antiphospholipid syndrome.
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9/95. Central retinal artery occlusion by proxy: a cause for sudden blindness in an airline passenger.

    The use of gas media in ophthalmologic procedures is relatively commonplace. Scleral buckle and pneumatic retinopexy procedures using air-gas mediums are a widely accepted treatment for retinal detachment. We present a patient who had a scleral buckle with pneumatic retinopexy performed and subsequently flew in a commercial airliner 2 wk later. The patient experienced sudden blindness due to central retinal artery occlusion brought about by expansion of the air bubble when the aircraft reached cruise altitude and a cabin pressure of 8000 ft. The intraocular pressure exceeded the central artery pressure thereby collapsing the artery. The patient's symptoms were relieved when an onboard flight surgeon identified the problem and the cabin pressure was reset to 2000 ft. Flying after an ophthalmic procedure that incorporates intraocular gas may have complications due to the bubble expansion in accordance with Boyle's Law. The ophthalmologic surgeon must be diligent in forewarning patients of the potential complications of flying for weeks to months after a procedure that utilizes intraocular gas.
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10/95. Superior orbital 'petrositis' and late ischaemic monocular blindness induced by intense UV radiation exposure.

    Many physical agents cause neuropathies. The most common are chronic pressure, vibration and temperature. In general, these lesions occur at work, as a result of accidents or through chronic exposure to the physical agent. radiation leading to peripheral neuropathy is also related to radiotherapy in cancer treatment, as an undesirable side-effect. We present here a case report of short, intense UV radiation exposure at work, leading to delayed-onset ocular neuropathy. A clear cause-effect relationship is shown, demonstrated using magnetic resonance imaging scans. We suggest that the mechanism was thermal and ischaemic.
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