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170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

14 cases of posterior ischemic optic neuropathy (PION) were clinically analyzed, in whom we excluded known etiologies of optic nerve disturbances and confirmed the decreased blood supply to the posterior portion of the optic nerve. On the basis of our clinical findings, we have proposed the following criteria for the diagnosis of idiopathic PION: (1) sudden onset of unilateral visual disturbance in older patients; (2) normal optic disc, subsequently developing simple optic atrophy; (3) hypertensive and arteriosclerotic changes in the retinal vessels; (4) varying degrees of impaired vision, variable visual field defects; (5) associated systemic disease such as hypertension, diabetes mellitus, hyperlipemia, hypotension, etc.; (6) exclusion of other demonstrable causes of optic nerve disturbances, and (7) confirmation of abnormal hemodynamics in the posterior portion of the optic nerve by carotid angiography, ophthalmodynamography, ophthalmodynamometry and fluorescein fundus angiography.
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PMID:Posterior ischemic optic neuropathy. III. Clinical diagnosis. 663 61

Ischemic optic neuropathy is a frequent cause of sudden visual loss in the older patient. There are two major causes of ischemic optic neuropathy; one, arteritic, due to an inflammatory process, and the other, idiopathic, possibly linked to hypertension. This paper presents four illustrative cases of ischemic optic neuropathy, one with an associated serous retinal detachment. The clinical appearance of the disorder, differential diagnosis of the two major types of ischemic optic neuropathy, and the pathogenesis and prognosis for vision are discussed. Currently accepted modes of treatment are also included.
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PMID:Arteritic and idiopathic ischemic optic neuropathy. 683 5

Based on the method of person-years, the morality rate of 155 patients with circulatory disorders was calculated and compared with the death rate of an age-matched general population. No excess mortality was found among 53 patients with central retinal vein occlusion and among 58 patients with ischemic optic neuropathy. On the other hand, 44 patients with central retinal or branch artery occlusion showed a statistically significant increased mortality rate. Patients with arterial circulatory disorders were subdivided into hypertensives and normotensives; an increased mortality rate was seen only among patients with hypertension but not among patients with normal blood pressure. Hypertension is one of the main cardiovascular risk factors. The increased mortality risk among our patients with hypertension may be indicative of a progressive atherosclerosis.
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PMID:[Life expectancy of patients with circulatory disorders of the posterior eyeball segment]. 687 59

This is a brief overview of multifaceted anatomical, experimental and clinical studies conducted by the author since 1955 on the optic nerve head circulation in health and disease. Conclusions, based on the accumulated information provided by these studies, are summarized. The studies on the pattern of blood supply of the optic nerve head have shown that: (a) its main source of blood supply is the posterior ciliary artery circulation, with retinal circulation supplying only the surface nerve fiber layer, (b) there is marked interindividual variation in the blood supply pattern, and (c) the blood supply in the optic nerve head has a sectorial distribution. The various factors which produce interindividual variation in the blood supply of the optic nerve head are discussed, particularly those in the posterior ciliary artery circulation; this is because all available evidence indicates that it is derangement in the posterior ciliary circulation in the optic nerve head that is primarily responsible for the common ischemic disorders of the optic nerve head, e.g. anterior ischemic optic neuropathy and glaucomatous optic neuropathy. Factors that may derange the blood flow in the optic nerve head include defective autoregulation of blood flow in it, vascular changes in its feeding arteries, hematologic abnormalities, systemic arterial hypertension and hypotension, and intraocular pressure; their roles are discussed. For better understanding and management of optic nerve head ischemic disorders, there is an urgent need for an accurate clinical method of assessment of blood flow in the posterior ciliary circulation in optic nerve head, since no satisfactory method is currently available. Redness or pallor of the optic disk on ophthalmoscopy is not a true guide to the optic nerve head vascularity as it gives no information about the state of the posterior ciliary circulation. Fluorescein fundus angiography, though far superior to the optic disk color for evaluation of optic nerve head vascularity, has a number of limitations. All these topics and various controversies about them are discussed briefly.
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PMID:The 1994 Von Sallman Lecture. The optic nerve head circulation in health and disease. 755 90

The diagnosis of optic neuritis is based on clinical signs and symptoms. Ancillary testing has little medical value, but is helpful to evaluate the risk of developing multiple sclerosis and for counseling the patients. In contrast to the common belief, the usual therapy with oral prednisone may be harmful. Only megadose therapy with 1000 mg methylprednisolone/day accelerates the recovery of visual function. Similar therapy is suggested in idiopathic intracranial hypertension. In patients with non-arteritic anterior ischemic optic neuropathy only optic nerve decompression sheath surgery is helpful.
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PMID:[Neuro-ophthalmology--new challenges]. 765 Aug 79

The pathogenesis of non-arteritic anterior ischemic optic neuropathy (AION) is not well understood. Local factors like elevated IOP or a low C/D ratio may play a role, as may systemic arteriosclerosis or reduced perfusion pressure. Reduced cardiac output may also contribute to the pathogenesis of the disease. We therefore investigated 17 healthy young persons, 9 patients with non-arteritic AION, and 10 age-matched controls using fluorescence perfusion scintigraphy, a technique that allows subclavia carotid time to be determined. Subclavia carotid time measures the circulation time of the heart and lung and is proportional to cardiac output. The mean subclavia carotid time of healthy young persons was 9.1 +/- 1.6 s, 9.9 +/- 1.9 for AION patients, and 9.9 +/- 1.2 s for age-matched controls. The differences were statistically not significant. The correlation of perfusion times with blood pressure values showed, however, that systemic hypertension is accompanied by a relatively slow systemic perfusion time. In conclusion, it was not possible to demonstrate an absolutely reduced cardiac output in patients with non-arteritic AION during the day. Nevertheless, a drop in systemic blood pressure during the night may be responsible for a reduction in the blood supply to the optic nerve.
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PMID:[Systemic perfusion times in non-arteritic anterior ischemic optic neuropathy]. 771 83

We measured 24-hour ambulatory blood pressure monitoring and diurnal curve of the intraocular pressure in 166 white patients with anterior ischemic optic neuropathy, normal-tension glaucoma, primary open-angle glaucoma, and other optic nerve head disorders. Hourly average blood pressure data analyses showed a significant (P < .0001) decrease in mean systolic (26%) and diastolic (33%) blood pressure measurements at night. A significantly (P = .0028) lower nighttime mean diastolic blood pressure and a significantly (P = .0044) greater mean percentage decrease in diastolic blood pressure were noted in normal-tension glaucoma than in anterior ischemic optic neuropathy. Patients with arterial hypertension taking oral hypotensive therapy showed a significant association between progressive visual field deterioration and nocturnal hypotension, particularly in anterior ischemic optic neuropathy. Intraocular pressure showed no significant correlation with visual field deterioration in any of these conditions. Our findings suggest that nocturnal hypotension, in the presence of other vascular risk factors, may reduce the optic nerve head blood flow below a critical level, and thereby may play a role in the pathogenesis of anterior ischemic optic neuropathy and glaucomatous optic neuropathy; that is, nocturnal hypotension may be the final insult in a multifactorial situation. The same mechanisms may be true of a number of other ocular ischemic disorders. This finding opens a new dimension in the understanding and management of these visually disabling diseases.
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PMID:Nocturnal arterial hypotension and its role in optic nerve head and ocular ischemic disorders. 817 67

Temporal arteritis is an insidious disease which, if not recognized and treated with high-dosage oral prednisone or intravenous prednisolone, can result in unilateral or even total blindness due to anterior ischemic optic neuropathy (AION) or closure of the central artery of the retina. Unfortunately, the symptoms and clinical signs of temporal arteritis mimic those of a number of other conditions including angle-closure glaucoma, hypertension, migraine, trigeminal neuralgia, temporomandibular joint syndrome, carotid artery occlusive disease, Foster-Kennedy syndrome, and nonarteritic AION. When a patient complains of a severe pain in the temporal region, along with scalp tenderness and a feeling of malaise or depression--with or without episodes of transient loss of vision--he or she should be referred for a diagnostic work-up which includes an erythrocyte sedimentation rate and a temporal artery biopsy. We present here a review of the recent literature concerning temporal arteritis, followed by a report of an unusual case in which high-dosage prednisone therapy was effective in relieving the patient's symptoms and lowering the sedimentation rate in spite of a negative temporal artery biopsy.
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PMID:Diagnosis and management of temporal arteritis: a review and case report. 823 73

The prevalence of diabetic ocular complications and the correlation between diabetic retinopathy and systemic factors were examined in 2,300 cases (4,600 eyes) with non-insulin-dependent diabetes mellitus. The prevalence of cataract was 66.7%, of retinopathy 37.0%, of refractive and accommodative change 6.2%, of glaucoma 1.9% (rubeotic glaucoma was 1.0%), of rubeosis iridis 1.5%, of iridocyclitis 0.8%, of extraocular muscle palsy 0.2%, and of ischemic optic neuropathy 0.1%. Duration of diabetes mellitus, HbA1C value, methods of diabetic control, age, diabetic nephropathy, diabetic neuropathy, hypertension, systolic blood pressure, diastolic blood pressure, and arteriosclerosis obliterans were related with diabetic retinopathy. We suggest that the management of diabetic patients needs sufficient attention in the cases with oral administration of medication, insulin therapy, and diabetic nephropathy.
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PMID:[Prevalence of diabetic ocular complications and systemic factors]. 836 83

This study was undertaken to understand better how damage to the anterior visual pathway may affect the relationship between the visual and pupillomotor systems. The relative afferent pupillary defect and the interocular difference in visual field mean deviation (determined by the Humphrey Field Analyzer Statpac program) were correlated in 137 patients. A moderate linear correlation (r = .66) was found. In 25 patients tested by both static and kinetic perimetry, the correlation could not be significantly improved by considering field loss outside of 30 degrees. The correlation was further studied in four subcategories of diagnosis: optic neuritis (n = 36), idiopathic intracranial hypertension (n = 26), compressive optic neuropathy (n = 14), and anterior ischemic optic neuropathy (n = 7). In compressive optic neuropathy and idiopathic intracranial hypertension, the difference in mean deviation between the two eyes was associated with a larger relative afferent pupillary defect than in optic neuritis and anterior ischemic optic neuropathy. In optic neuritis, the correlation was the poorest. These results indicate that diseases of the afferent visual system may not necessarily affect visual threshold (as tested by static perimetry) and the pupillary light reflex (a suprathreshold test) in the same way.
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PMID:The relationship between static perimetry and the relative afferent pupillary defect. 844 95


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