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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three patients with visual loss and normal fundi were discovered to have choroidal ischemia on fluorescein angiography. Each patient had a markedly increased Westergren erythrocyte sedimentation rate, but only one described symptoms of polymyalgia rheumatica, neck pain, and jaw claudication. Biopsy of the temporal artery confirmed giant cell arteritis in the two patients without constitutional symptoms. In one patient, typical anterior ischemic optic neuropathy developed the following day, whereas in the other two, anterior ischemic optic neuropathy later occurred despite the prompt administration of intravenous high-dose corticosteroids. Choroidal ischemia may be the first sign of giant cell arteritis in elderly patients with visual loss. Early diagnosis and treatment are mandatory in an attempt to forestall the development of anterior or posterior ischemic optic neuropathy, or central retinal artery occlusion in the affected or fellow eye.
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PMID:Visual loss caused by choroidal ischemia preceding anterior ischemic optic neuropathy in giant cell arteritis. 829 97

A 68-year-old man had visual loss secondary to isolated choroidal nonperfusion as a clinical manifestation of giant cell arteritis. Ophthalmoscopy disclosed scattered yellow-white lesions at the level of the retinal pigment epithelium in the posterior pole of the right eye. Intravenous fluorescein angiography demonstrated marked delay in choroidal filling of the macula in the right eye. There was no ophthalmoscopic or angiographic evidence of anterior ischemic optic neuropathy or central retinal artery occlusion. After approximately 72 hours of intravenous corticosteroid therapy, the patient's visual acuity improved and repeat intravenous fluorescein angiography showed normal choroidal circulation. Isolated choroidal ischemia is a potential cause of reversible visual loss in patients with giant cell arteritis.
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PMID:Choroidal nonperfusion in giant cell arteritis. 835 1

We present five patients who developed luxury perfusion following anterior ischemic optic neuropathy in whom fluorescein angiography was misinterpreted as "capillary hemangioma" or neovascularization of the disc. In each case, the segment of disc hyperemia corresponded to a spared region of visual field. Luxury perfusion represents a reparative autoregulatory reaction to ischemia.
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PMID:Luxury perfusion following anterior ischemic optic neuropathy. 886 7

Non-arteritic anterior ischemic optic neuropathy (AION-na) classically presents with visual loss, altitudinal visual field defects, and optic nerve swelling. AION-na presumably occurs secondary to an ischemic event. Two patients are described who were at risk for developing AION-na. Both patients presented with optic disc edema but did not have visual loss or visual field defects. Neither patient developed visual loss or visual field defects in the affected eye throughout one and two years of follow-up respectively. The optic disc edema resolved spontaneously in both affected eyes. The clinical spectrum of AION-na could range from a "full-blown" classic attack to a minimal attack characterized by disc swelling without visual loss. The amount and distribution of disc ischemia determines the individual clinical picture. The failure of either affected eye in this study to develop symptoms likely represents a graded axonal atrophy with mechanical decompression of the optic nerve.
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PMID:Asymptomatic optic disc edema. 909 57

Giant cell (temporal) arteritis continues to be a sight-threatening, systemic vasculitis with a poorly understood pathogenesis. The characteristic granulomatous inflammation of the vessel wall commonly leads to local ischemia. Recent advances in immunological investigations have characterized the cellular components of the disease process, but the etiology has so far remained unresolved. A reappraisal of the clinical features of giant cell (temporal) arteritis demonstrates the heterogeneity of the manifestations of the disease, including ischemic optic neuropathy. A range of new laboratory investigations and blood flow studies with color Doppler imaging have demonstrated promising roles, with respect to diagnosis and long-term follow-up. Prompt diagnosis and expeditious treatment require a high index of clinical suspicion, particularly for atypical cases. Corticosteroids remain the treatment of choice, other immuno-suppressive agents being used as second line steroid-sparing agents. Giant cell (temporal) arteritis leads to increased vascular and visual morbidity and, if untreated, may prove fatal. To maintain high standards of management of this enigmatic disorder, ophthalmologists need to be aware of the clinical spectrum of giant cell (temporal) arteritis and currently available diagnostic tests and treatment strategies.
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PMID:Current concepts in giant cell (temporal) arteritis. 938 74

Loss of retinal ganglion cells (RGCs) is a hallmark of many ophthalmic diseases including glaucoma, retinal ischemia due to central artery occlusion, anterior ischemic optic neuropathy and may be significant in optic neuritis, optic nerve trauma, and AIDS. Recent research indicates that neurotoxicity is caused by excessive stimulation of receptors for excitatory amino acids (EAAs). In particular, the amino acid glutamate has been shown to act as a neurotoxin which exerts its toxic effect on RGCs predominantly through the N-methyl-D-aspartate (NMDA) subtype of glutamate receptor. NMDA-receptor-mediated toxicity in RGCs is dependent on the influx of extracellular Ca2+. The increase in [Ca2+]i acts as a second messenger that sets in motion the cascade leading to eventual cell death. Glutamate stimulates its own release in a positive feedback loop by its interaction with the non-NMDA receptor subtypes. Ca(2+)-induced Ca2+ release and further influx of Ca2+ through voltage-gated Ca2+ channels after glutamate-induced depolarization contribute to glutamate toxicity. In vitro and in vivo studies suggest that the use of selective NMDA receptor antagonists or Ca2+ channel blockers should be useful in preventing or at least abating neuronal loss in the retina. Of particular importance for future clinical use of NMDA receptor antagonists in the treatment of acute vascular insults is the finding that some drugs can prevent glutamate-induced neurotoxicity, even when administered a few hours after the onset of retinal ischemia.
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PMID:Molecular basis of glutamate toxicity in retinal ganglion cells. 942 25

Tobacco smoke is composed of as many as 4,000 active compounds, most of them toxic on either acute or long-term exposure. Many of them are also poisonous to ocular tissues, affecting the eye mainly through ischemic or oxidative mechanisms. The list of ophthalmologic disorders associated with cigarette smoking continues to grow. Most chronic ocular diseases, with the possible exception of diabetic retinopathy and primary open-angle glaucoma, appear to be associated with smoking. Both cataract development and age-related macular degeneration, the leading causes of severe visual impairment and blindness, are directly accelerated by smoking. Other common ocular disorders, such as retinal ischemia, anterior ischemic optic neuropathy, and Graves ophthalmopathy, are also significantly linked to this harmful habit. Tobacco smoking is the direct cause of tobacco-alcohol amblyopia, a once common but now rare disease characterized by severe visual loss, which is probably a result of toxic optic nerve damage. Cigarette smoking is highly irritating to the conjunctival mucosa, also affecting the eyes of nonsmokers by passive exposure (secondhand smoking). The dangerous effects of smoking are transmitted through the placenta, and offspring of smoking mothers are prone to develop strabismus. Efforts should be directed toward augmenting the campaign against tobacco smoking by adding the increased risk of blindness to the better-known arguments against smoking. We should urge our patients to quit smoking, and we must make them keenly aware of the afflictions that can develop when smoke gets in our eyes.
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PMID:The association between cigarette smoking and ocular diseases. 963 2

One of the most susceptible sites to vascular diseases is the optic nerve head. By innovative approaches using morphometry and in situ hybridization, vascular and extracellular characteristics of the human optic nerve head were examined. Nonarteritic ischemic optic neuropathy occurs due to vascular insufficiency within the optic nerve head. Various local and systemic risk factors have been proposed among which smoking and acute hypotension are now included. Anatomically abnormal discs such as the small optic disc, tilted disc, and optic nerve drusen are recognized as "disks at risk" and hyperopia may be an additional predisposing factor. Ocular, neurological, and vascular disorders due to giant cell arteritis were reviewed. Intravenous high-dose methylprednine should be administered in certain cases. Differentiating nonarteritic from arteritic ischemic optic neuropathy is sometimes difficult. Isolated choroidal ischemia or choroidal filling delay may be an indication of giant cell arteritis. Studies have been conducted on the vascular event, amaurosis fugax (transient monocular visual loss), and the results of some of these studies are discussed.
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PMID:Neuro-ophthalmic aspects of vascular disease. 1015 Aug 24

It is widely suspected that tissue ischemia initiates or participates in optic disk damage in glaucoma. The details are not well delineated. Particularly puzzling is the clear separation of the clinical appearances of glaucoma and anterior ischemic optic neuropathy, which is also a presumed ischemic disease. When venous pressure at the exit point from the eye is elevated by intraocular pressure (IOP), the arteriovenous pressure difference is reduced. Nutrition is maintained only because of blood flow autoregulation. Intraocular pressure-induced ischemia can result if autoregulation is impaired in an individual, either because of an innate deficiency or, perhaps, as a result of vasospastic disease. Autoregulation can also be impaired if another disease (e.g., an atheroma) has caused much of the autoregulatory capacity to be already utilized, so that little or none is left to respond to the additional challenge of IOP. Ischemia might also result from microvascular occlusion with platelet or clotting abnormalities, perhaps inducing glaucomatous optic neuropathy that is not dependent on IOP. A better understanding of the pathogenic mechanism (and how it may be different in various cases) is needed to predict more successfully an individual's risk of glaucomatous damage, to make decisions about the aggressiveness of treatment, and, one day, to direct therapy at the type of vascular abnormality present, in addition to or instead of lowering IOP.
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PMID:Introductory comments on blood flow autoregulation in the optic nerve head and vascular risk factors in glaucoma. 1041 42

Acute visual loss secondary to ischemic optic neuropathy in children is extremely rare. The causes are usually hypotension or anemia. We describe the clinical course of a 9-year-old boy with a functional renal transplant who presented to the emergency room hemodynamically stable after waking up with complete bilateral loss of vision (no light perception). Examination showed that he had suffered massive nocturnal blood loss from esophageal varices secondary to portal hypertension. The patient's end-stage renal disease was secondary to autosomal recessive polycystic kidney disease (ARPKD), an entity comprised of renal cysts and hepatic fibrosis. Ophthalmologic findings in ARPKD are rarely cited in the literature. A literature search revealed 3 other cases of sudden visual loss reported in nonophthalmologic journals in patients with ARPKD. Funduscopic examination showed bilateral optic nerve head pallor and swelling with associated flame hemorrhages. The fact that this patient already had mildly pale nerves on presentation, along with hemodynamically compensated blood pressure and pulse, suggested chronic as well as acute ischemia. Based on our findings and other reported cases in the literature, ophthalmologic examinations may be indicated in all patients with ARPKD.
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PMID:Acute visual loss in a child with autosomal recessive polycystic kidney disease: case report and review of the literature. 1282 65


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