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1/59. Bilateral posterior ischemic optic neuropathy after spinal surgery.

    PURPOSE: To report the association between bilateral posterior ischemic optic neuropathy and spinal surgery. METHOD: Case report. RESULTS: After prone-position spinal surgery of 8 hours' duration, a 68-year-old woman was completely blind in both eyes. Moderate periorbital edema and temporal conjunctival chemosis were present bilaterally. Ophthalmic examination disclosed normal-appearing optic nerve heads, except for bilateral nasal fullness related to bilateral optic nerve drusen, and no retinal edema. Immediate cerebral arteriography, magnetic resonance imaging, and electroretinography were normal. Visual-evoked response was not detectable, and 7 weeks later, severe bilateral optic nerve head pallor developed. CONCLUSIONS: Severe selective hypoperfusion of the retrobulbar optic nerves may occur after spinal surgery. pressure to the periorbital region may be a contributing factor.
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2/59. Acute unilateral visual loss due to a single intranasal methamphetamine abuse.

    An otherwise healthy 35 year old male with insulin-dependent diabetes mellitus (IDDM) presented himself three days after a single intranasal methamphetamine abusus. Directly upon awakening the day after the recreational use of this drug, he discovered an acute and severe visual loss of his right eye. This unilateral loss of vision was permanent and eventually lead to a pale and atrophic optic nerve head. The characteristics of this visual loss, together with the aspect of the optic nerve head was very similar to the classical non-arteritic ischemic optic neuropathy (NAION). We suggest a direct ischemic episode to the short posterior ciliary arteries due to this single intranasal abuse of methamphetamine as the underlying pathogenesis of this acute and permanent visual loss.
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3/59. Bilateral simultaneous optic nerve dysfunction after periorbital trauma: recovery of vision in association with with chiropractic spinal manipulation therapy.

    OBJECTIVE: To discuss the recovery of optic nerve function after chiropractic spinal manipulation in a patient with loss of vision as a result of facial fracture from a fall. CLINICAL FEATURES: In a fall down a stairwell, a 53-year-old woman with migraines fractured her right zygomatic arch, which was later treated surgically. Approximately 3 weeks after the accident, vision in her contralateral eye became reduced to light perception. Electrophysiologic studies revealed that the function of both optic nerves was diminished, the right significantly more than the left. Single photon emission tomography showed pancerebral ischemic foci. INTERVENTION AND OUTCOME: chiropractic spinal manipulation was used to aid recovery of vision to normal over a course of 20 treatment sessions. At times, significant improvement in vision occurred immediately after spinal manipulation. Progressive recovery of vision was monitored by serial visual field tests and by electrophysiologic studies. Unfortunately, the patient refused a further single photon emission tomographic study when visual recovery was complete. CONCLUSION: This case report adds to previous accounts of progressive and expeditious recovery of optic nerve function in association with spinal manipulation therapy.
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4/59. The diagnostic challenge of occult large vessel ischemia of the retina and choroid.

    Vascular occlusions of the retina and choroid can cause severe visual loss. These occlusions can occur as a result of systemic disease or after surgery. In most cases, the retinal appearance provides evidence of ischemia as the cause of visual loss. On occasion, however, clinical examination shows no objective signs of vascular occlusion, and this can lead the clinician to suspect optic nerve pathology as the cause of visual loss. This paper outlines some of the diagnostic criteria, clinical findings, and ancillary studies that can be used to differentiate between occult occlusion of the retina or choroid and optic nerve disease.
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5/59. Loss of vision from distant haemorrhage: report of four cases.

    To describe the occurrence of visual loss from ischaemia of the optic nerve following distant haemorrhages. Four patients who sustained vision loss following distant haemorrhage, presenting to the neuro-ophthalmic clinic of the department of ophthalmology, Addis Ababa University, from 1995 to 1997 were evaluated. The clinical presentation, management and prognosis are discussed. Post-haemorrhagic vision loss, other than being a rare occurrence, is under-reported due to the fact that these patients are very sick with massive blood loss and hence little attention is given to the vision loss by attending physicians and sometimes even the patients themselves. It is hoped that this paper will increase awareness about this condition among physicians attending to patients with severe bleeding and thus facilitate early diagnosis and referral.
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6/59. giant cell arteritis causing bilateral sequential anterior ischaemic optic neuropathy--a case report.

    giant cell arteritis is a chronic granulomatous inflammation of unknown aetiology involving large and medium size arteries in the elderly. It causes acute visual loss from ischaemia to the optic nerves or central retinal artery occlusion. This is a rare cause of anterior ischaemic optic neuropathy in our local population. We present a patient who had bilateral loss of vision from sequential arteritic ischaemic optic neuropathy. She was treated with intravenous steroids immediately. Diagnosis was based on histopathological studies of temporal artery biopsies.
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7/59. Anterior ischaemic optic neuropathy associated with central retinal vein occlusion.

    PURPOSE: To report the unusual association between non-arteritic anterior ischaemic optic neuropathy (NAION) and non-ischaemic central retinal vein occlusion (CRVO) in two patients. methods: case reports are presented. RESULTS: Non-ischaemic CRVO was manifested by dilated, tortuous retinal veins with flame-shape retinal haemorrhages. fluorescein angiography showed prolonged arteriovenous transit time and normal retinal capillary perfusion without macular oedema. The presence of colour vision abnormalities, relative afferent pupillary defects, pale disc swelling and visual field deficits indicated that the visual loss was attributable entirely to NAION. Laboratory investigations disclosed impaired fibrinolytic function in case 1 and the presence of antiphospholipid antibodies in case 2. CONCLUSIONS: Compression of the central retinal vein by the swollen optic nerve could have predisposed to CRVO. The presence of thrombophilic abnormalities may have contributed to the concomitant occlusion of posterior ciliary arteries and central retinal vein. Ischaemic optic neuropathy needs to be considered in patients with CRVO when the visual acuity is not consistent with the retinal pathology.
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8/59. Atypical features prompting neuroimaging in acute optic neuropathy in adults.

    BACKGROUND: Acute optic neuropathy due to an intracranial lesion may masquerade as optic neuritis or nonarteritic anterior ischemic optic neuropathy (NAION). We reviewed the records of patients who presented with acute unilateral optic neuropathy that was initially diagnosed as optic neuritis or NAION but who ultimately proved to have an underlying structural lesion. methods: Retrospective observational case series. We reviewed the records of patients with the initial diagnosis of optic neuritis or NAION in whom the diagnosis was changed to an intracranial etiology at four tertiary care neuro-ophthalmology centres between 1995 and 1998. RESULTS: Eight cases were identified in which atypical features prompted further investigation, including neuroimaging, leading to the diagnosis of an intracranial etiology for the optic neuropathy. Five patients were discovered to have neoplasms (a tuberculum sellae meningioma in two cases, an optic nerve sheath meningioma in two cases and a metastatic lesion in one case), and three patients had intracranial sarcoidosis. Atypical features for optic neuritis included a progressive course, absence of pain, optic atrophy at presentation, lack of significant visual improvement and age over 40 years. For NAION, the atypical features included progressive course, optic atrophy on presentation, absence of vasculopathic risk factors and preceding transient visual loss. INTERPRETATION: Clinicians should be aware that patients with intracranial lesions may present with acute optic neuropathy mimicking optic neuritis or NAION and that certain atypical features should warrant consideration for neuroimaging.
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9/59. Axonal loss in a patient with anterior ischemic optic neuropathy as measured with scanning laser polarimetry.

    PURPOSE: To report Nerve Fiber Analyzer (NFA/GDx; Laser Diagnostic Technologies, San Diego, california) measurements in a patient during the early phase of an anterior ischemic optic neuropathy. methods: Case report. A 58-year old man with acute anterior ischemic optic neuropathy had repeated NFA/GDx scans of the nerve fiber layer adjacent to the optic nerve head of the involved eye, as well as repeated HFA 30.2 (Humphrey Field Analyzer; Humphrey Systems, San Leandro, california) visual field examinations. RESULTS: At presentation (day 0), he had a normal superior nerve fiber bundle on the NFA/GDx, with a deep inferior hemifield scotoma. By day 21 and day 36, the superior nerve fiber bundle thinned on the NFA/GDx, whereas the scotoma remained practically unchanged. CONCLUSION: These findings suggest that after the onset of an anterior ischemic optic neuropathy, acute loss of axonal function results in scotoma, presumably from ischemia. This is followed by a gradual disappearance of nerve fiber tissue, as measured with the NFA/GDx, within several weeks.
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10/59. 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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