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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors have investigated risk factors associated with the occurrence of nonarteritic anterior ischemic optic neuropathy (AION) in 83 patients and 124 eyes. 12% of the patients with nonarteritic AION had diabetes mellitus, 37.3% hypertension, 14.5% atherosclerosis, while the rest (36.2%) were classified as idiopathic. The incidence of bilateral AION was slightly less than 50%. The period in which both eyes get affected is usually 1-2 months or longer. Nonarteritic AION can occur at any age, therefore it is seen in young people as well. The role of arterial hypertension and diabetes in pathogenesis of AION is still to be determined.
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PMID:Risk factors in nonarteritic anterior ischemic optic neuropathy. 207 25

The records of 293 patients admitted to Padua University Eye Clinic with diagnosis of optic neuropathy were reviewed. Age and sex distribution of different types of optic neuropathies were analyzed. 84 patients (28.7%) with a mean age of 61.9 years had anterior ischemic optic neuropathy (AION). The mean follow up of these patients was 3 years. In less than 30% of patients stabilized visual acuity of the first affected eye was better than 20/200; however, patients younger than 65 showed a significantly (p less than 0.01) better visual acuity than patients older than 64. Involvement of the second eye was found in 26 patients with AION (30.9%), of whom only five were considered idiopathic. The latency before controlateral eye involvement was significantly (p less than 0.05) shorter in patients over 64 years of age than in the younger group. Commonly known associated conditions such as giant cell arteritis (3.6%), arterial hypertension (34.5%), diabetes mellitus (10.7%), both arterial hypertension and diabetes (8.3%), migraine (7.2%) or intracapsular cataract extraction (1.2%) were considered. The frequency of a number of risk factors was found out in patients with arterial hypertension and/or diabetes and in patients with idiopathic AION. Symptoms or signs of ischemic cardiopathy and/or peripheral nonarteritic vascular disease, TIAs prior to AION onset, elevated plasma cholesterol or triglyceride levels, excessive smoking were considered. These risk factors were not found in 11.1% of diabetic patients with AION, in 37.9% of hypertensives, in 14.2% of both diabetic and hypertensive patients and in 31% of patients with idiopathic AION. Our data seem to indicate that the onset of AION may be influenced more strongly from these risk factors than aging.
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PMID:Anterior ischemic optic neuropathy and aging. 277 May 22

Electroretinograms (ERG), oscillatory potentials (OP) and pattern reversal visual evoked potentials (VEP) were performed in nine patients (mean age 66 years) with unilateral long-standing anterior ischemic optic neuropathy (AION) and in an age matched control group. Normal ERGs but bilateral impaired OPs were observed in virtually all AION affected patients. Regardless of visual acuity, VEP amplitude reduction was found in all eyes with AION and in controlateral eyes of patients with associated systemic conditions such as diabetes mellitus, arterial hypertension and atherosclerosis. A normal latency of VEP was found bilaterally in AION affected patients; however no correlation between VEP latency and visual acuity or fields could be established. Our results seem to indicate moderate ischemic damage to the retina and to the axons of the optic pathways in patients with AION.
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PMID:Electrophysiological findings in anterior ischemic optic neuropathy. 277 May 27

A 63-year-old white male with mild hypertension, peptic ulcer disease, and anxiety was diagnosed as having nonarteritic anterior ischemic optic neuropathy (AION). The patient presented with unilateral disc edema and a paracentral scotoma. Follow-up examination at 10 weeks revealed resolution of the scotoma. This is one of a few cases in which remission of the visual field defect has been reported.
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PMID:Remission of visual field loss in nonarteritic anterior ischemic optic neuropathy. 372 43

We produced experimental renovascular arterial hypertension in 57 rhesus monkeys by modified Goldblatt's procedures. Hypertensive fundus changes were studied in detail by serial ophthalmoscopy and fluorescein fundus angiography in all animals on a long-term follow-up, and pathologically in 23 eyes. Initial evidence of hypertensive optic neuropathy was optic disc edema which developed at the median blood pressure (BP) of 190 mmHg (normal BP, 120 mmHg). On follow-up, mild to marked pallor of the optic disc developed. The optic disc changes were correlated with BP and other fundus changes. Pathogenesis of hypertensive optic neuropathy, which has been highly controversial so far, is discussed at length in the light of the findings of the present study and other recent evidence. All the available clinical and pathologic findings in the present study indicate that hypertensive optic neuropathy represents a form of anterior ischemic optic neuropathy, and that hypertensive optic neuropathy is a distinct entity. A caution is given against a precipitous reduction of BP in patients with hypertensive optic neuropathy because that may cause complete, permanent blindness.
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PMID:Fundus lesions in malignant hypertension. V. Hypertensive optic neuropathy. 395 18

Ischemic optic neuropathy occurred in three patients (a 55-year-old man and two women, 64 and 68 years old). Visual loss followed coronary bypass surgery in two patients who also had diffuse atherosclerotic disease. Retinal emboli were present in both eyes of each. The third patient developed ischemic optic neuropathy with evidence of ipsilateral retinal emboli shortly after cardiac catheterization. Her only other risk factor for ischemic optic neuropathy was systemic hypertension. Although highly unusual, ischemic optic neuropathy may be associated with and possibly caused by a shower of emboli to the eye.
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PMID:Ischemic optic neuropathy associated with retinal embolism. 400 98

Of 217 patients in whom anterior ischemic optic neuropathy (AION) was diagnosed during the period from 1975 to 1985, verifiable medical information was obtained for 212 (98%). Over a median follow-up period of three years, no group of patients had an increased mortality rate over that of age-, sex-, and race-matched controls; however, patients with "idiopathic" AION and patients with systemic hypertension who developed nonarteritic AION had a statistically significant increased risk of experiencing cerebrovascular events and myocardial infarctions compared with appropriately matched control groups. In view of the findings of our study, we suggest that patients with idiopathic AION and hypertensive patients who develop nonarteritic AION undergo a complete physical examination, cardiac evaluation, tests of carotid artery patency, and careful medical follow-up to attempt to prevent subsequent cerebrovascular or cardiovascular events.
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PMID:The risk of cerebrovascular and cardiovascular disease in patients with anterior ischemic optic neuropathy. 402 42

Accelerated renovascular hypertension produces optic nerve changes ranging from optic disc edema to optic atrophy. To elucidate the pathogenesis of hypertensive optic neuropathy, the optic nerves from 12 monkeys (23 eyes) with accelerated renovascular systemic hypertension were studied by electron and light microscopy. Within 21 months, the animals demonstrated the entire spectrum of pathologic changes. In the optic nerves with optic disc edema, the prelaminar optic nerve exhibited vasoconstriction with subsequent axonal hydropic swelling, axolemma disruption, and glial swelling. In retrolaminar myelinated optic nerve, vasoconstriction was more severe, with endothelial swelling and pericytic degeneration resulting in intramyelinic vacuoles and glial swelling. Optic disc edema appeared to result from axonal hydropic swelling secondary to ischemic infarct, followed by loss of axons and gliosis in the prelaminar optic nerve. The retrolaminar myelinated nerve showed prominent microglial reaction and eventual atrophy of axons and glia. Ischemia seemed to play a major role in hypertensive optic neuropathy, which represents anterior ischemic optic neuropathy.
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PMID:Fundus lesions in malignant hypertension. II. A pathologic study of experimental hypertensive optic neuropathy. 402 51

Two monocular normotensive patients with nonarteritic ischemic optic neuropathy and retinal ischemia unresponsive to steroid therapy were treated with intravenous norepinephrine. In both patients, improvement in vision began within minutes after moderate hypertension was produced. A third patient showed no response to this therapy in one eye with established ischemic optic neuropathy, but had prompt recovery of vision in the second eye early in the course of ischemic optic neuropathy. This patient returned with recurrent ischemic optic neuropathy more than 1 year later. At that time she was found to have essential hypertension. One patient could not be weaned from the norepinephrine infusion without recurrent visual loss. In the second patient, controlled hypertensive therapy restored visual acuity to 20/30 during two separate recurrences of ischemic optic neuropathy. Therapy of a later episode of ischemic optic neuropathy was delayed for 2 days, and vision did not improve with norepinephrine infusion. This eye subsequently became painful and required enucleation. Histopathological evaluation showed combined arterial and venous occlusions within the optic nerve and evidence of previous peripapillary choroidal vascular occlusion. Selected normotensive patients with ischemic optic neuropathy and retinal ischemia may benefit from controlled hypertensive therapy induced by norepinephrine infusion.
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PMID:Norepinephrine therapy of ischemic optic neuropathy. 621 76

Of 196 patients with anterior ischemic optic neuropathy, 169 had the nonarteritic form and 27 had the arteritic type. Visual acuities were 20/40 or better in 83 of 184 eyes with nonarteritic anterior ischemic optic neuropathy but only eight of 45 eyes with the arteritic type. We found systemic disease associations for hypertension and diabetes mellitus only for patients with nonarteritic anterior ischemic optic neuropathy who were between 45 and 64 years of age. After a mean follow-up period of five years, 92 nonarteritic patients showed no changes in the first affected eye; there was eventual involvement of the second eye in 20 patients.
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PMID:Clinical profile and long-term implications of anterior ischemic optic neuropathy. 662 29


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